Tonsillitis

Anatomy and pathogenesis

Inflammation in tonsillitis unfolds within Waldeyer's lymphoid ring. This is an important barrier organ of the immune system, comprising the palatine, lingual, pharyngeal, and tubal tonsils. Although the palatine tonsils take the primary hit, the entire lymphoid ring reacts concomitantly. Enlargement and tenderness of the regional lymph nodes (cervical and submandibular) are an obligatory accompaniment to the inflammation.

The clinical picture includes pain upon swallowing, fever, and symptoms of intoxication. Autoinfection acts as the leading development factor. Bacteria penetrate the tissue transepithelially or return via the hematogenous route. Hypothermia or a general drop in the body's resistance usually serves as the trigger. Transmission of infection from outside occurs via airborne droplets or alimentary routes.

The main causative agent is group A hemolytic streptococcus (S. pyogenes). Staphylococci (S. aureus, S. capitis), fusobacteria (F. necrophorum, inhabiting the gingival pockets, genitals, and intestines), and various anaerobes (C. perfringens, C. histoliticum, C. septicum) are less common.

Clinical and anatomical forms of acute tonsillitis

Pathological anatomy distinguishes several variants of the course 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 in the folds (lacunae). Macroscopically, these are yellowish masses protruding above the hyperemic surface. Microscopically, infiltration of the lacunar epithelium by neutrophils, the formation of erosions, and the adhesion of fibrin threads to the exudate are visible.
• Follicular: lymphoid follicles hyperplasticize and suppurate, turning into microabscesses. They shine through the mucosa as millet-seed-sized yellowish grains.
• Fibrinous: develops in diphtheria. The necrotic mucosa is deeply impregnated with fibrin (diphtheritic inflammation), forming a tightly adherent film.
• Phlegmonous: arises due to diffuse infiltration of the entire lymphoepithelial tissue of the tonsil by neutrophilic leukocytes.
• Necrotic: necrosis of the covering epithelium dominates with the formation of a grayish coating consisting of tissue detritus, leukocytes, decay products, and fibrin. The outcome consists in the rejection of necrotic masses. Extensive erosions form in their place, which can deepen down to the pharyngeal walls, turning into ulcers. The healing of such defects is always accompanied by the formation of coarse scars.

Special types of tonsillitis

In addition to classical forms, specific variants are distinguished:

1. Plaut-Vincent angina (Simanovsky-Plaut-Vincent tonsillitis): an ulceromembranous form caused by F. necrophorum infection. Superficial defects covered with a dirty-greenish coating form on the mucosa. The presence of a pronounced putrid odor is characteristic.
2. Ludwig's angina: a severe process triggered by anaerobic microflora from carious cavities or periodontal pockets. Necrosis starts in the lymphoepithelial tissue and rapidly spreads to the tissues of the floor of the mouth. A characteristic feature is the dominance of necrotic changes over signs of inflammatory infiltration. Macroscopically, foul-smelling "meat-water" colored fluid and gas bubbles are discovered in the muscles and adipose tissue, giving the classical picture of anaerobic gangrene.

Chronic tonsillitis

If bacterial antigens constantly stimulate the immune system, sensitization occurs, and the process becomes chronic. The dynamics of changes in lymphoid tissue in this case go through two stages: at first, hyperplasia is observed, which is subsequently replaced by atrophy and sclerosis.

A chronic focus of infection in the tonsils harbors the threat of both local and systemic complications. Local purulent processes include parapharyngeal (peritonsillar) abscess and neck phlegmon. The spread of infection via vessels can cause thrombophlebitis and sepsis. In addition, the body's sensitization by antigens triggers pathological reactions leading to the development of rheumatic fever and glomerulonephritis.

Class and exam questions

What else to study on this topic

• Mechanisms of sensitization in chronic tonsillitis
• Pathogenesis of the development of rheumatic fever and glomerulonephritis
• Differential diagnosis of diphtheritic and necrotic tonsillitis
• Morphological changes in lymph nodes in acute tonsillitis
• Anaerobic gangrene of the soft tissues of the face and neck (using Ludwig's angina as an example)

Other topics in the «Digestive System Diseases» section

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