Anatomy and Pathogenesis
Inflammation in tonsillitis unfolds within Waldeyer's ring, an essential barrier organ of the immune system that includes the palatine, lingual, pharyngeal, and tubal tonsils. Although the palatine tonsils bear the brunt of the infection, the entire lymphoid ring reacts cooperatively. Enlargement and tenderness of regional lymph nodes (cervical and submandibular) are constant companions of this inflammation.
Clinical manifestations include odynophagia (pain on swallowing), fever, and systemic intoxication. The leading pathogenetic factor is autoinfection. Bacteria penetrate the tissue transepithelially or return via hematogenous routes. Hypothermia or a general drop in body resistance usually serves as the trigger. Transmission from external sources occurs via airborne droplets or food-borne routes.
The primary pathogen is group A beta-hemolytic streptococcus (S. pyogenes). Less common pathogens include staphylococci (S. aureus, S. capitis), fusobacteria (F. necrophorum, residing in gingival pockets, genitalia, and the intestine), and various anaerobes (C. perfringens, C. histoliticum, C. septicum).
Clinical and Anatomic Forms of Acute Tonsillitis
Pathological anatomy distinguishes several variants of the acute process:
- Catarrhal: characterized by inflammatory hyperemia of the pharyngeal tonsils and the mucosa of the palatine arches.
- Lacunar: seropurulent or mucopurulent exudate accumulates within the folds (lacunae) of the tonsils. Macroscopically, these appear as yellowish masses protruding above the hyperemic surface. Microscopically, neutrophil infiltration of the lacunar epithelium, erosion formation, and the deposition of fibrin strands within the exudate are observed.
- Follicular: lymphoid follicles hyperplasticize and undergo suppuration, turning into microabscesses. They shine through the mucosa as millet-seed-like yellowish granules.
- Fibrinous: develops in diphtheria. The necrotic mucosa is deeply infiltrated by fibrin (diphtheritic inflammation), forming a tightly adherent pseudomembrane.
- Phlegmonous: arises due to diffuse infiltration of the entire lymphoepithelial tissue of the tonsil by neutrophil leukocytes.
- Necrotic: necrosis of the surface epithelium dominates, forming a grayish coating composed of tissue debris, leukocytes, breakdown products, and fibrin. The outcome involves the sloughing of necrotic masses. Extensive erosions form in their place, which may deepen into the pharyngeal wall to become ulcers. Healing of such defects is invariably accompanied by the formation of coarse scars.
Special Types of Tonsillitis
In addition to classic forms, specific variants are distinguished:
- Plaut-Vincent angina (Fusospirochetal tonsillitis): an ulceromembranous form caused by F. necrophorum infection. Superficial defects covered by a dirty-greenish coating form on the mucosa. A pronounced putrid odor is characteristic.
- Ludwig's angina: a severe process triggered by anaerobic microflora originating from carious cavities or periodontal pockets. Necrosis initiates in the lymphoepithelial tissue and rapidly spreads to the tissues of the floor of the mouth. A key feature is the dominance of necrotic changes over signs of inflammatory infiltration. Macroscopically, a foul-smelling, 'dishwater' fluid and gas bubbles are found within the muscles and adipose tissue, presenting a classic picture of anaerobic gangrene.
Chronic Tonsillitis
If bacterial antigens continually stimulate the immune system, sensitization develops, and the process becomes chronic. The dynamics of lymphoid tissue changes progress through two stages: initial hyperplasia, which is subsequently replaced by atrophy and sclerosis.
Chronic foci of infection within the tonsils harbor threats of both local and systemic complications. Local purulent processes include peritonsillar abscess and neck phlegmon. The vascular spread of infection can cause thrombophlebitis and sepsis. Furthermore, systemic sensitization to antigens triggers pathological immune-mediated reactions leading to rheumatic fever and glomerulonephritis.