Complications of acute tonsillitis

Local (purulent) complications

Local complications are associated with the breakthrough of infection beyond the tonsillar capsule. The classic chain of pus spread is as follows: peritonsillar abscess (paratonsillitis) → retropharyngeal abscess or parapharyngitis → neck phlegmon → purulent mediastinitis.

The most common condition is a peritonsillar abscess. It occurs shortly after a previous bout of tonsillitis or due to problems with the eruption of the third molar ("wisdom tooth hood" sign).

Clinical presentation of the abscess:

• Acute unilateral sore throat radiating to the ear;
• Inability to swallow food and water;
• Trismus: marked spasm of the masticatory muscles;
• Fever up to 39–40 °C, severe chills, insomnia;
• Nasally voice, hypersalivation, fetid breath, and an earthy complexion.

During pharyngoscopy, the physician observes asymmetry of the soft palate, displacement of the tonsil toward the midline, and tissue bulging. Based on the localization of the abscess within the tissue, they are classified as anterosuperior, anteroinferior, posterior, and lateral. The lateral abscess is considered the most dangerous due to the high risk of inflammation spreading to the parapharyngeal space.

Treatment requires emergency care. Before the abscess forms, broad-spectrum antibiotics are administered (exclusively via injection, as the patient cannot swallow pills due to trismus), along with antihistamines, warm neck compresses, and warm gargles (nitrofural, potassium permanganate). Antipyretics (acetylsalicylic acid) and analgesics (metamizole sodium) are used for symptom relief. A formed abscess requires surgical drainage.

Systemic (metatonsillar) complications

General complications develop due to the body's systemic response to the infection. Tonsillocardiac syndrome (rheumatism and heart damage) ranks first in frequency, followed by kidney damage (tonsillorenal syndrome), joint involvement, gastrointestinal tract disorders, hematopoietic organ disorders, and the development of sepsis.

Chronic streptococcal processes induce persistent sensitization in the body. If the infection is caused by rheumatogenic M-serotypes of Group A beta-hemolytic Streptococcus, an autoimmune reaction—acute rheumatic fever—is triggered.

A rheumatic attack affects various systems:

• Heart: rheumatic endocarditis and myocarditis. Clinical signs of heart involvement usually come to the fore on days 5–7, after joint pains subside.
• Joints: migratory polyarthritis of large symmetrical joints. The process is exudative in nature and heals without severe deformations or scars (involvement of the temporomandibular joint is possible).
• Kidneys: focal or diffuse glomerulonephritis.
• Other organs: rheumatic pneumonia, polyserositis.

Morphologically, this process manifests as the formation of specific rheumatic granulomas, microcirculatory vasculitis, and nonspecific exudative reactions.

It is important to distinguish rheumatic kidney damage from acute post-streptococcal glomerulonephritis. The latter is caused by a distinct group of nephritogenic streptococcal strains and develops via an immune complex mechanism (immune complexes deposit directly in the renal glomeruli rather than damaging them through direct invasion).

Streptococcal virulence factors and diagnostics

The pathogen's ability to cause severe complications and chronic disease is due to its potent pathogenic factors:

• M-protein of the cell wall is the main virulence factor. It inhibits bacterial phagocytosis by macrophages and triggers the production of antibodies that begin to attack the body's own tissues via molecular mimicry.
• Streptolysins O and S: activate the conversion of plasminogen to plasmin, dissolving fibrin.
• C5a peptidase: destroys chemotaxis factors, reducing the local immune response.
• Pneumolysin: directly damages target cell membranes.
• Hyaluronidase: helps bacteria easily move through connective tissue.

Persistence of infection and epidemic outbreaks are often associated with the formation of streptococcal L-forms (their reversion causes relapses) and mutations in genes encoding the M-protein.

Throat culture and serological tests are used for laboratory confirmation of the streptococcal nature of complications. The combination of high titers of ASO (antistreptolysin O) with anti-DNase B or antihyaluronidase has the highest diagnostic value.

Specifics of complications in scarlet fever

Scarlet fever is an acute form of infection caused by Streptococcus pyogenes in individuals lacking antitoxic immunity. Erythrogenic pyogenic exotoxins, acting as superantigens, play a key role in its pathogenesis.

Complications of scarlet fever are clearly divided by their time of onset:

1. Early complications: associated with direct bacterial invasion of tissues. These include necrotizing lymphadenitis, fasciitis, peritonsillar abscess, and generalized streptococcal sepsis.
2. Late complications (1–4 weeks later): have an autoimmune nature (molecular mimicry, immune complex deposition). These include acute rheumatic fever, post-streptococcal glomerulonephritis, arthritis, and vasculitis.

An extremely severe course of infection can lead to a fatal outcome due to infectious-toxic shock, acute cardiovascular failure against the background of rheumatic pancarditis, or cerebral edema.

Class and exam questions

What else to study on this topic

• Surgical technique for draining a peritonsillar abscess
• Pathogenesis of acute rheumatic fever and molecular mimicry
• Neck phlegmon and purulent mediastinitis: pathways of infection spread
• Mechanisms of streptococcal L-form formation and their role in relapses
• Differential diagnosis of tonsillitis and scarlet fever

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