Chronic Tonsillitis
Persistent low grade inflammation of the tonsils with continuous rather than episodic symptoms, distinguished from recurrent acute tonsillitis by the absence of symptom free intervals.
Pathophysiology
The tonsillar crypts, which number 10 to 30 per tonsil and which extend deep into the parenchyma, become chronically colonised. Three processes maintain the condition:
- Crypt obstruction by debris, desquamated epithelium and bacteria, forming an anaerobic environment.
- Biofilm formation on the crypt epithelium, in which organisms exist in a protected extracellular polymeric matrix that resists both antibiotic penetration and host immune clearance. Biofilms are demonstrable in the great majority of chronically inflamed tonsils and explain the failure of repeated antibiotic courses.
- Fibrosis of the tonsillar capsule and parenchyma, with scarring that obliterates crypt drainage and perpetuates the cycle.
Tonsilloliths
Concretions formed within the crypts from trapped debris, food, desquamated epithelium and bacteria, which calcify over time with deposits of calcium, phosphorus, magnesium and ammonium. Anaerobic organisms within them produce volatile sulphur compounds, which are the cause of the characteristic halitosis. They are a specific and frequently underestimated cause of distress, since patients are commonly told nothing is wrong.
Microbiology
Polymicrobial, with anaerobes predominating: Fusobacterium, Prevotella, Porphyromonas, Peptostreptococcus and Actinomyces. Aerobes include Staphylococcus aureus, Haemophilus influenzae, Moraxella catarrhalis and streptococci. Beta lactamase production by these organisms inactivates penicillin within the crypt environment.

