Acute nonspecific tonsillitis

Acute nonspecific angina is a disease that affects children of preschool and school age and adults (less often) up to 35-40 years. There are marked seasonal rises in the spring and autumn periods. Angina is 1.5-2 times more often sick in large cities with developed public transport than in small towns and rural areas.

According to the data of BS Perevozhensky (1956), acute nonspecific angina is a very common disease, as evidenced by the average statistical incidence of angina in the USSR for 1954 (39.17 cases per 1000 inhabitants). The increase in the incidence of sore throat is affected by the crowding of large groups (in kindergartens, schools, hostels, army units), especially in newly created groups, when cross-infection of their members with appropriate microorganisms occurs. A significant role in this is played by unfavorable ecological conditions, and some industrial hazards (atmospheric, radiation, etc.).

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10]

Epidemiology

Infection with pathogenic microorganisms in case of angina disease occurs in two ways - exogenous and endogenous. The first route includes airborne and alimentary infection. With airborne infection, the incidence of acute nonspecific angina in large groups has the character of local "epidemics". The alimentary pathway is possible with the use of infected foods, in particular milk from cows suffering from streptococcal udder disease. Equally, this applies to infants, nursing mothers who suffer from mastitis.

Endogenous infection occurs with the weakening of general and local immunity against a background of certain risk factors - local and general cooling, vitamin deficiency, protein deficiency in the diet (amino acid starvation), occupational and household hazards, allergies. In this case, the saprophytic microorganisms of the individual acquire pathogenic properties, causing an inflammatory process in the corresponding structures of the pharynx, which is of an infectious-allergic nature. Great importance in the emergence of endogenous infection is attached to chronic tonsillitis. In this case, recurrent or recurrent acute nonspecific angina is common, characteristic of the decompensated form of this disease of the palatine tonsils. As noted by B.S. Preobrazhensky (1954), the frequency of angina in chronic tonsillitis is explained by the fact that in this disease there is usually up to 75% of cases the carriage of a potentially virulent microbiota, especially hemolytic streptococcus, vegetating in the crypts of palatine tonsils.

[11], [12], [13], [14], [15], [16]

What causes acute nonspecific angina?

In the most common forms of angina (catarrhal, follicular and lacunar) as their pathogens are various pyogenic cocci (streptococcus, staphylococcus, pneumococcus), as well as yeast-like fungi of the genus Candida and others. An anaerobic infection can play an important role in the onset of acute nonspecific angina, adenoviruses, influenza viruses, as well as symbiosis with other pathogens. The source of infection can be purulent diseases of the nose and paranasal sinuses.

In the pathogenesis of angina, predisposing factors play a significant role, such as local and general hypothermia, overheating, harmful chemical and dusty atmospheric agents, a decrease in the reactivity of the organism, hypo- and avitaminosis, and sometimes a mechanical trauma (for example, a fish bone injection) of the palatine tonsil. Pathogenesis is closely related pathological changes, the nature of which is determined by the clinical forms of angina. The most common are the so-called vulgar (usual, banal) acute nonspecific angina. As mentioned above, there are also the anginas arising in acute infectious diseases (measles, scarlet fever, diphtheria, etc.), blood diseases (agranulocytosis, lymphatic leukemia, etc.), and special forms of angina, for example, Simanovsky-Plaut-Vincent's angina. For each of these forms is characteristic of its own pagaloanatomical picture.

Immunological characteristics

The disease with vulgar angina does not create any kind of permanent immunity, more often on the contrary (autoallergization and cross-sensitization): after the transferred angina follows a sequence of angina, caused by other microorganisms. On the one hand, this is due to a decrease in immunity as a result of angina, and on the other, to the phenomenon of sensitization of the local lymphadenoid formations of the pharynx to coccal antigens and the development in the body of allergic preparedness to respond to both endogenous and exogenous microorganisms. In other words, acute nonspecific angina opens wide gates for introduction into the body and activation of pathogenic microorganisms, which in some cases cause not only the occurrence of local relapses, but also the common infectious and allergic status, manifested by pathological processes in the interstitial and connective tissue (rheumatoid arthritis, endo - and myocarditis, other forms of collagenosis).

Among vulgar angina, catarrhal, follicular, lacunar and phlegmonous are distinguished.