Angina (acute tonsillitis): causes and pathogenesis

Causes of sore throat

Among the bacterial pathogens, a beta-hemolytic group A streptococcus is the determining factor, which causes angina in 15-30% of cases of acute tonsillopharyngitis in children and in 5-10% of cases in adults. The causative agent is transmitted by airborne droplets; The source of infection usually becomes sick or carriers, if there is close contact or a high degree of seeding. Outbreaks are more frequent in autumn or in spring. Staphylococcal infection is not seasonal, cases of the disease are recorded throughout the year.

The cause of angina may be other pathogens, such as pneumococci, intestinal and pseudomonas aeruginosa, spirochetes, fungi. There are various ways of infection, the penetration of the pathogen and the mucous membrane of the tonsils by airborne, alimentary, by direct contact. Probably also autoinfection by bacteria or viruses, vegetating on the mucous membrane of the pharynx and tonsils.

Mycoplasma and chlamydia as a cause of angina are found in children in 10-24% of cases, and in children under 2 years with acute tonsillitis, these microorganisms occur twice as often as beta-hemolytic streptococcus group A (in 10% and 4 5% of children, respectively ).

Among the clinical forms of angina in the daily practice of a doctor are more frequent diseases, referred to as "banal" (or vulgar) angina. The cause of angina of this form are cocci and in some cases adenoviruses. For banal angina is characterized by a number of clear pharyngoscopic features that distinguish them from other forms; there are also similar signs of organism intoxication; pathological changes in both palatine tonsils are determined; the duration of the course of the pathological process in these forms is usually within 7 days. The division of banal angina into separate forms of the clinical point of view is conditional. In essence, this is a single pathological process that has a similar course. Catarrhal angina is clinically milder and as an independent disease is infrequent.

[1], [2], [3], [4], [5], [6]

Other causes of sore throat

The pathogenesis of angina is based on the fact that the effect of the pathogen on the mucosa 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 determining the resistance of the organism are untenable. In the pathogenesis of angina, a certain role is played by a decrease in the adaptive abilities of the organism to cold, sharp seasonal fluctuations in environmental conditions (temperature, humidity, gas content, etc.). Alimentary factor (monotonous protein food with a lack of vitamins C and B) can also contribute to the formation of angina. A predisposing factor may be a trauma to the tonsils, a constitutional tendency to sore throats (for example, in children with a lymphatic-hyperplastic constitution).

Angina 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. Significantly more angina is seen in preschool and school children, as well as in adults up to 30-35 years. In the elderly, sore throat arises rarely and usually proceeds erased. This is explained by age-related involuntary changes in the lymphadenoid tissue of the pharynx.

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

With streptococcal etiology of angina associated with a high probability of late complications with the defeat of internal organs. In the stage of reconvalescence (on the 8th-10th day after the onset of the disease) post-streptococcal glomerulonephritis, toxic shock, may develop, and rheumatic fever after 2-3 weeks after relief of symptoms of tonsillitis.

Staphylococcal angina also has a number of characteristic features associated with the characteristics of the pathogen. Staphylococci, as one of the causes of angina, are extremely destructive microorganisms that cause abscesses; they secrete a variety of toxins, including antifagocytic factors, including the coagulase enzyme and protein A, which blocks opsonization. A typical place of penetration of staphylococcal infection is the mucous membrane of the nasal cavity, mouth and pharynx. At the site of the pathogen the primary purulent-inflammatory focus develops, in the mechanism of limitation of which the reaction of the regional lymph nodes is of great importance. Enzymes, secreted by staphylococci, promote the multiplication of microbes in the inflammatory focus and their spread into tissues by lymphogenous and hematogenous pathways. In the place of introduction of the pathogen an inflammatory process develops, for which the zone of necrosis and hemorrhagic exudate surrounded by leukocyte infiltration and congestion of staphylococci are characteristic. Possible formation of microabscesses with subsequent merging into large foci.

Pathomorphological changes in angina depend on the form of the disease. For all forms of angina characterized by a pronounced expansion of small blood and lymphatic vessels of the mucosa and parenchyma of the tonsils, fompoz of small veins and stasis in the lymphatic capillaries.

In catarrhal sinus the mucous membrane is hyperemic, full-blooded, swollen, impregnated with a serous secret. The epithelial covering of the tonsils on the surface and in the crypts is densely infiltrated by lymphocytes, neutrophils. In some places the epithelium is loosened and desquamated. There are no purulent raids.

In the follicular form of angina, the morphological picture is characterized by more pronounced changes in the parenchyma of the tonsils, with predominantly follicular damage. They appear leukocyte infiltrates, and in some there is necrosis. On the surface of edematous, hyperemic tonsils, the festering follicles appear through the epithelial cover in the form of yellow, purulent dots. With microscopy, follicles with purulent fusion are revealed, as well as hyperplastic follicles with light centers.

Lacunar angina is characterized by congestion in the enlarged lacuna initially serous-purulent, and then purulent exudate, consisting of leukocytes, cells of the ejaculated epithelium, fibrin. Microscopically detected ulceration of the epithelium lacunae, infiltration of the mucous membrane by leukocytes, thrombosis of small vessels and foci of purulent fusion in the follicles. The exudate emerges from the mouths of the lacunae in the form of whitish yellowish corks and islets of fibrinous plaque on the surface of the brightly hyperemic and edematic tonsils. The raids from the mouths of the lacuna tend to spread and connect with the neighboring ones, forming wider drainage raids.

Ulcerative necrotic angina is characterized by the spread of necrosis to the epithelium and parenchyma of the amygdala. The tonsils are covered with a whitish-gray coating consisting of necrotic tissue, leukocytes, a large number of bacteria, fibrin. The raids are then softened and torn off, forming ulcers with uneven edges. The propagation of the necrotic process over the surface and in the depth of the tissues can lead to the destruction of the soft palate and the penny of the pharynx, followed by scarring of the defect. The cervical lymph nodes are involved in the process. Necrotic angina is more common in acute leukemia and other diseases of the blood system, perhaps with scarlet fever, diphtheria. Complications such as hemorrhage or gangrene are possible. For the Simanovsky-Plaut-Vincent angina, surface ulceration is more common, covered with a dirty gray coating with putrefactive odor on one amygdala, while the second amygdala does not have such changes.

With herpetic sore throat, serous exudate forms small subepithelial vesicles, which, bursting, leave defects in the epithelial lining. Simultaneously, the same vesicles can appear on the mucous membrane of the lingual-lingual and palatine-pharyngeal arch, soft palate.

With phlegmonous tonsillitis (intratonsillar abscess), lacunar drainage is broken, the amygdala parenchyma is initially edematous, then infiltrated by leukocytes, necrotic foci in the follicles, merging form an abscess inside the amygdala. Such an abscess can be located close to the surface of the amygdala and emptied into the oral cavity or into the paratonsillar tissue.

The patient, regardless of what causes of angina, and who suffered this disease, does not form stable immunity, especially with streptococcal etiology of the disease. Conversely, in the period of convalescence, relapse of the disease is often possible. This is also due to the fact that pathogens can be various types of microorganisms. After the transferred adenoviral tonsillitis remains type-specific immunity, which does not guarantee protection from a similar disease caused by another type of adenovirus.