Complications of tonsillitis

Local (purulent) complications

Purulent complications develop when the inflammatory process extends beyond the palatine tonsils. Classically, these include:

• Peritonsillar abscess — rupture of pus beyond the tonsillar capsule into the surrounding paratonsillar tissue.
• Retropharyngeal abscess.
• Parapharyngitis.

If the purulent process is not resolved, the infection may spread down the interfascial spaces. This poses a risk of cervical phlegmon (cultures frequently reveal staphylococci, streptococci, enterobacteria, and non-spore-forming anaerobes). Further tracking of pus leads to a severe condition — purulent mediastinitis, where staphylococci and enterobacteria are frequent pathogens, while streptococcus and pneumococcus are rare.

General complications and pathogenesis of rheumatism

Chronic streptococcal tonsillitis or pharyngitis leads to persistent sensitization of the body. This creates the basis for the development of acute rheumatic fever (rheumatism). It is important to remember that only certain M-serotypes of GABHS possess rheumatogenic properties (1, 3, 5, 6, 14, 18, 19, 24).

Autoimmunization and host tissue damage are driven by potent pathogenicity factors of streptococcus:

• M-protein of the cell wall is the main virulence factor. It inhibits macrophage phagocytosis and stimulates the production of type-specific antibodies that cross-react with human tissues.
• C5a peptidase — destroys the chemotactic factor, reducing the influx of immune cells.
• Streptolysins O and S — activate the conversion of plasminogen to streptokinase, leading to plasmin generation and fibrinolysis.
• Hyaluronidase — a "spreading factor" enzyme that facilitates bacterial movement through connective tissue.
• Pneumolysin — damages target cell membranes.

Persistence of the pathogen in the body is often associated with the formation of streptococcal L-forms. Their reversion to the initial bacterial form triggers new attacks of rheumatism. In addition, epidemic outbreaks of the disease may be explained by mutations in the emm genes encoding the M-protein.

Clinical and morphological picture of a rheumatic attack

During the development of rheumatism, virtually all organs can be involved in the pathological process. Morphologically, this is manifested by the formation of Aschoff (rheumatic) granulomas and non-specific exudative-proliferative reactions (infiltrates of lymphocytes, macrophages, sometimes eosinophils and neutrophils), as well as microcirculatory vasculitis.

Main clinical manifestations:

1. Heart involvement: rheumatic endocarditis and myocarditis. Cardiac symptoms usually come to the forefront on days 5–7, after the joint syndrome subsides.
2. Joint involvement: rheumatic migratory polyarthritis. Large symmetrical joints are affected (including the temporomandibular joint). The process is predominantly exudative in nature, which is why healing occurs without gross scarring and deformation.
3. Other systems: rheumatic pneumonia, polyserositis.

Post-streptococcal glomerulonephritis

Acute post-streptococcal (proliferative) glomerulonephritis is an independent renal complication. It is caused by specific, nephritogenic GABHS strains that differ from rheumatogenic ones.

The pathogenesis of this complication is fundamentally different: renal tissue damage occurs not due to direct bacterial invasion, but via an immune complex mechanism. Immune complexes (antigen-antibody) deposit in the glomeruli, triggering severe inflammation.

Laboratory diagnostics and follow-up

To confirm the streptococcal etiology of complications, clinicians use throat cultures for group A Streptococcus and antibody titer assessment. The combination of ASO with anti-DNase B or antihyaluronidase has the highest sensitivity.

Patients who have suffered from rheumatic carditis are subject to strict dispensary observation to prevent relapses and the progression of heart defects. In the first year, examinations are carried out monthly, and quarterly thereafter. If such a patient contracts an intercurrent infection (tonsillitis), they are mandatorily prescribed:

• Complete blood count (CBC) and urinalysis on the 14th and 21st days of the illness.
• ECG on the 21st day.

This is necessary for the timely detection of latent carditis or glomerulonephritis.

Class and exam questions

What else to study on this topic

• Mechanisms of streptococcal persistence: the role of L-forms and emm gene mutations
• Morphology of the rheumatic process: granulomas and vasculitis
• Pathogenicity factors of GABHS at the molecular level
• Specific and general inflammatory laboratory markers of tonsillopharyngitis
• Secondary prevention of acute rheumatic fever in children

Other topics in the "Additional Topics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.