Angina (acute tonsillitis) - Causes and pathogenesis

Causes of angina

Among bacterial pathogens, the leading role belongs to beta-hemolytic streptococcus group A, which is the cause of sore throat in 15-30% of cases of acute tonsillopharyngitis in children and in 5-10% of cases in adults. The pathogen is transmitted by airborne droplets; the source of infection is usually the patient or carriers, if there is close contact or a high degree of contamination. Outbreaks of the disease are most often observed in the fall or spring. Staphylococcal infection has no seasonality, cases of the disease are registered throughout the year.

Other pathogens such as pneumococci, intestinal and pseudomonas aeruginosa, spirochetes, and fungi can also cause tonsillitis. Various infection routes are possible: penetration of the pathogen into the mucous membrane of the tonsils by airborne droplets, alimentary route, or direct contact. Autoinfection with bacteria or viruses vegetating on the mucous membrane of the pharynx and tonsils is also possible.

Mycoplasmas and chlamydia as a cause of tonsillitis occur in children in 10-24% of cases, and in children under 2 years of age with acute tonsillitis, these microorganisms occur twice as often as beta-hemolytic group A streptococcus (in 10% and 4.5% of children, respectively).

Among the clinical forms of angina in the daily practical activity of a doctor, diseases designated as "banal" (or vulgar) angina are more common. The cause of angina of this form are cocci and, in some cases, adenoviruses. Banal angina is characterized by the presence of a number of clear pharyngoscopic signs that distinguish them from other forms; there are also similar signs of intoxication of the body; pathological changes are determined in both palatine tonsils; the duration of the pathological process in these forms is usually within 7 days. The division of banal angina into separate forms from a clinical point of view is conditional. In essence, this is a single pathological process that has a similar course. Catarrhal angina clinically proceeds more mildly and is rarely encountered as an independent disease.

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Other causes of sore throat

The pathogenesis of tonsillitis is based on the fact that the effect of the pathogen on the mucous membrane of the palatine tonsils can lead to the development of the disease only if, under the influence of external and internal factors, local and general protective mechanisms that determine the body's resistance prove ineffective. In the pathogenesis of tonsillitis, a certain role is played by a decrease in the body's adaptive capacity to cold, sharp seasonal fluctuations in environmental conditions (temperature, humidity, gas pollution, etc.). The alimentary factor (monotonous protein food with a lack of vitamins C and group B) can also contribute to the development of tonsillitis. A predisposing factor may be trauma to the tonsils, a constitutional tendency to tonsillitis (for example, in children with a lymphatic-hyperplastic constitution).

Tonsillitis as an independent disease is relatively rare in infants and young children, when the lymphadenoid apparatus of the pharynx is not yet developed, but at this age it is severe, with pronounced general manifestations. Tonsillitis is much more often observed in preschool and school-age children, as well as in adults up to 30-35 years old. In old age, tonsillitis occurs rarely and usually proceeds in an erased manner. This is explained by age-related involutional changes in the lymphadenoid tissue of the pharynx.

The development of angina occurs as an allergic-hyperergic reaction. It is assumed that the rich microflora of the tonsil lacunae and protein breakdown products can act as substances that promote sensitization of the body. In a sensitized organism, various factors of exogenous or endogenous nature can cause angina. In addition, an allergic factor can serve as a prerequisite for the development of complications such as rheumatism, acute nephritis, nonspecific infectious polyarthritis and other diseases of an infectious-allergic nature. The most pathogenic are beta-hemolytic streptococci of group A. They carry capsules (M-protein) for attachment to mucous membranes (adhesion), are resistant to phagocytosis, secrete numerous exotoxins, cause a strong immune response, and also contain antigens that cross-react with the heart muscle. In addition, immune complexes that include them are involved in kidney damage.

Streptococcal etiology of tonsillitis is associated with a high probability of developing late complications with damage to internal organs. In the recovery stage (on the 8th-10th day from the onset of the disease), post-streptococcal glomerulonephritis, toxic shock may develop, and rheumatic fever may develop 2-3 weeks after the relief of tonsillitis symptoms.

Staphylococcal tonsillitis also has a number of characteristic features associated with the characteristics of the pathogen. Staphylococci, as one of the causes of tonsillitis, are extremely destructive microorganisms that cause abscesses; they secrete many toxins, including antiphagocytic factors, including the enzyme coagulase and protein A, which blocks opsonization. A typical site of penetration of staphylococcal infection is the mucous membrane of the nasal cavity, mouth and pharynx. At the site of penetration of the pathogen, a primary purulent-inflammatory focus develops, in the mechanism of limiting which the reaction of regional lymph nodes is of great importance. Enzymes secreted by staphylococci promote the proliferation of microbes in the inflammatory focus and their spread to tissues by lymphogenous and hematogenous routes. At the site of pathogen introduction, an inflammatory process develops, characterized by a necrosis zone surrounded by leukocyte infiltration and accumulation of staphylococci and hemorrhagic exudate. Microabscesses may form, subsequently merging into large foci.

Pathological changes in angina depend on the form of the disease. All forms of angina are characterized by a sharply expressed expansion of small blood and lymphatic vessels of the mucous membrane and parenchyma of the tonsils, phombosis of small veins and stasis in the lymphatic capillaries.

In catarrhal tonsillitis, the mucous membrane is hyperemic, full-blooded, swollen, and soaked with serous secretion. The epithelial covering of the tonsils on the surface and in the crypts is densely infiltrated with lymphocytes and neutrophils. In some places, the epithelium is loosened and desquamated. There are no purulent deposits.

In the follicular form of tonsillitis, the morphological picture is characterized by more pronounced changes in the parenchyma of the tonsils, with follicles being predominantly affected. Leukocyte infiltrates appear in them, with necrosis observed in some. On the surface of the edematous, hyperemic tonsils, suppurating follicles are visible through the epithelial cover in the form of yellow purulent dots. Microscopy reveals follicles with purulent melting, as well as hyperplastic follicles with light centers.

Lacunar tonsillitis is characterized by accumulation of initially serous-purulent and then purulent exudate in the enlarged lacunae, consisting of leukocytes, cells of desquamated epithelium, and fibrin. Microscopically, ulceration of the epithelium of the lacunae, infiltration of the mucous membrane with leukocytes, thrombosis of small vessels, and foci of purulent melting in the follicles are detected. The exudate emerges from the mouths of the lacunae in the form of whitish-yellowish plugs and islets of fibrinous plaque on the surface of a brightly hyperemic and edematous tonsil. The plaque from the mouths of the lacunae tends to spread and merge with neighboring plaques, forming wider confluent plaques.

Ulcerative necrotic tonsillitis is characterized by the spread of necrosis to the epithelium and parenchyma of the tonsil. The tonsils are covered with a whitish-gray coating consisting of necrotic tissue, leukocytes, a large number of bacteria, and fibrin. The coating subsequently softens and is rejected, forming ulcers with jagged edges. The spread of the necrotic process over the surface and deep into the tissues can lead to the destruction of the soft palate and penny pharynx with subsequent scarring of the defect. The cervical lymph nodes are involved in the process. Necrotic tonsillitis is more often observed in acute leukemia and other diseases of the blood system, and can occur with scarlet fever and diphtheria. Complications such as hemorrhages or gangrene are possible. Simanovsky-Plaut-Vincent's angina is most often characterized by superficial ulcerations covered with a dirty-gray coating with a putrid odor on one tonsil, while the second tonsil does not have such changes.

In herpetic angina, serous exudate forms small subepithelial vesicles, which, when bursting, leave defects in the epithelial lining. At the same time, the same vesicles can appear on the mucous membrane of the palatoglossal and palatopharyngeal arches, and the soft palate.

In phlegmonous tonsillitis (intratonsillar abscess), the drainage of the lacunae is disrupted, the parenchyma of the tonsil is initially edematous, then infiltrated with leukocytes, necrotic foci in the follicles, merging, form an abscess inside the tonsil. Such an abscess can be localized close to the surface of the tonsil and empty into the oral cavity or into the paratonsillar tissue.

The patient, regardless of the causes of the sore throat, and having suffered this disease, does not develop a stable immunity, especially with streptococcal etiology of the disease. On the contrary, during the recovery period, relapses of the disease are often possible. This is also explained by the fact that pathogens can be different types of microorganisms. After suffering adenoviral sore throat, type-specific immunity remains, which does not guarantee protection from a similar disease caused by another type of adenovirus.