Local (purulent) complications
Purulent complications develop when infection spreads by contact beyond the tonsils. Classical local complications include:
- Peritonsillar abscess — breakthrough of purulent inflammation beyond the tonsillar capsule with melting of the peritonsillar tissue.
- Retropharyngeal abscess.
- Parapharyngitis.
As parapharyngitis progresses, pus can spread to the fascial spaces of the neck, forming neck phlegmon. In these cases, the causative agents include not only streptococci, but also staphylococci, Enterobacteriaceae, or non-spore-forming anaerobes. Subsequently, purulent masses can descend along the interfascial spaces into the mediastinum, leading to life-threatening purulent mediastinitis.
Streptococcal pathogenicity factors
Chronic tonsillitis or pharyngitis of streptococcal etiology causes persistent bodily sensitization. This forms the foundation for acute rheumatic fever. The bacterium's ability to evade immunity and damage tissues is due to a rich arsenal of virulence factors:
- M-protein — a key cell wall protein. It inhibits macrophage phagocytosis and stimulates antibody production. Mutations in its encoding gene emm often trigger epidemic outbreaks.
- Streptolysins O and S — trigger the conversion of plasminogen into streptokinase, generating plasmin, which dissolves fibrin barriers.
- C5a peptidase — destroys the chemotactic factor, preventing leukocytes from migrating to the lesion site.
- Pneumolysin — destroys host cell membranes.
- Hyaluronidase and DNase — degrade connective tissue, ensuring deep invasion into structures.
Protracted course and relapses are also associated with the formation of streptococcal L-forms. The bacterium persists in this form, and upon reverting to the normal form, triggers a new rheumatic attack.
Autoimmune complications: rheumatic attack
Acute rheumatic fever affects connective tissue throughout the body. At the macroscopic and clinical levels, this manifests as a complex of syndromes:
- Rheumatic myocarditis and endocarditis — cardiac symptoms usually come to the forefront on days 5–7, immediately after the inflammation in the joints subsides.
- Migratory polyarthritis — predominantly affects large, symmetrical joints (occasionally the temporomandibular joint). The process is strictly exudative in nature, so no deformations or scars remain after inflammation subsides.
- Rheumatic pneumonia and polyserositis.
The morphological basis of these changes consists of specific rheumatic granulomas, as well as nonspecific exudative-proliferative reactions (accumulations of lymphocytes, macrophages, isolated neutrophils, and eosinophils in the interstitium) and vasculitis in the microcirculatory system.
Post-streptococcal glomerulonephritis
Unlike rheumatic fever, acute proliferative post-streptococcal glomerulonephritis is caused by a separate group of microorganisms — nephritogenic strains of GAS. The pathogenesis of this complication is not associated with direct bacterial damage to the glomeruli. Renal tissue damage occurs via an immune complex-type hypersensitivity mechanism: circulating antigen-antibody complexes deposit in the glomeruli, triggering a potent inflammatory response.
Laboratory diagnostics and follow-up
To confirm the diagnosis, throat swab culture and serological tests are used. The rise in titers of specific antibodies is evaluated: ASO, anti-DNase B, antihyaluronidase, and antistreptokinase. The combination of ASO with anti-DNase B has the highest sensitivity.
It is important to remember that the peak concentration of ASO occurs 2–4 weeks after tonsillitis. Therefore, this test is not applicable for the acute diagnosis of tonsillitis — it is needed exclusively for retrospective confirmation of infection when late autoimmune complications develop.
Children who have suffered from rheumatic carditis are placed under follow-up dispensary observation (monthly in the first year, then quarterly). If such a patient falls ill with tonsillitis or pharyngitis again, they are prescribed strict monitoring: CBC and urinalysis on the 14th and 21st days, as well as an ECG on the 21st day, so as not to miss a latent relapse of carditis or glomerulonephritis.
The differences of rheumatic polyarthritis are easy to remember: "L-S-M" joints — Large, Symmetrical, Migratory. At the same time, the inflammation is strictly exudative, so no deformations remain after the attack.
Class and exam questions
Can streptococcal tonsillitis be diagnosed solely by the ASO level?
No. The ASO titer reaches its maximum only 2–4 weeks after the onset of the disease. This test is used retrospectively to link an already developed complication (e.g., rheumatic fever) with a previously sustained infection.
Why do joints get affected in rheumatic fever, but disability rarely occurs?
In rheumatic polyarthritis, the inflammatory process in the joints is predominantly exudative in nature, without pronounced proliferation of connective tissue cells. Therefore, healing occurs without a trace, without the formation of rough scars and deformations.
Do the same strains of streptococcus cause rheumatic fever and glomerulonephritis?
No. Rheumatic fever is caused by so-called rheumatogenic M-serotypes (1, 3, 5, 6, 14, 18, 19, 24), while kidney damage is caused by specific nephritogenic strains of the microorganism.
What else to study on this topic
- Structure and functions of the streptococcal cell wall M-protein
- Morphology of the specific rheumatic granuloma
- Mechanism of formation and role of bacterial L-forms in chronic persistence
- Immune-complex mechanism of renal glomeruli damage
- Scarlet fever: impact of erythrogenic toxin on pathogenesis
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