Causes and pathogenesis of chronic tonsillitis

Palatine tonsils are part of the immune system, which consists of three barriers: lympho-blood (bone marrow), lympho-interstitial (lymph nodes) and lympho-elithelial (lymphoid aggregations, including tonsils, in the mucous membrane of various organs: pharynx, larynx, trachea and bronchi, intestines). The mass of palatine tonsils constitutes an insignificant part (about 0.01) of the lymphoid apparatus of the immune system.

The cause of chronic tonsillitis is a pathological transformation (the development of chronic inflammation) of the physiological process of the formation of immunity in the tissues of the palatine tonsils, where the normally limited inflammation process stimulates the production of antibodies.

Causes of chronic tonsillitis

In the palatine tonsils contact infection with immunocompetent cells that produce antibodies. Lymphoid tissue is permeated with numerous cracks - crypts, the walls of which are covered with 3-4 layers of epithelium, in many places the islets of epithelium are absent (sections of the so-called physiological angiosis). Through these de-epithelialized islets, the microorganisms penetrate the crypts and contact the tonsil cells. Each palatine tonsil contains 18-20 crypts, penetrating its parenchyma and, moreover, tree-branching. The surface area of the walls of all crypts is enormous: about 300 cm ² (the pharyngeal area, for example, is 90 cm ² ). Crypts penetrate the microflora from the mouth and pharynx, and from the parenchyma of the tonsils - lymphocytes. Microorganisms enter the amygdala not only through de-epithelialized islands, but also through the epithelium of the crypt walls, forming a limited, so-called physiological, inflammation in the parietal region. Live microorganisms, their dead bodies and toxins are antigens that stimulate the formation of antibodies. Thus, in the walls of crypts and lymphoid tissue of the amygdala (along with the entire mass of the immune system), normal immune mechanisms are formed. These processes are most active in childhood and young age. The immune system of the body normally keeps the activity of physiological inflammation in the tonsils at a level not more than sufficient to form antibodies to various microbial agents entering the crypts. Due to certain local or common causes, such as hypothermia, viral and other diseases (especially repeated angina), weakening immunity, physiological inflammation in the tonsils is activated, virulence and the aggressiveness of microbes in the crypts of the tonsils increase. Microorganisms overcome the protective immune barrier, limited physiological inflammation in the crypts becomes pathological, extending to the parenchyma of the amygdala. Autoradiographic study of tonsils in a healthy person and in a patient with chronic tonsillitis confirms the formation of a foci of infection during the development of the disease.

Among the bacterial flora that constantly grows in the palatine tonsils and causes the emergence and development of chronic tonsillitis under certain conditions, there may be streptococci, staphylococci and their associations, as well as pneumococci, influenza rod, etc. These microorganisms begin to colonize the tonsils immediately after the birth of the child, strains can be different: from 1 month to 1 year.

In the development of chronic tonsillitis and its complications, an important role is played by beta-hemolytic streptococcus of group A and greening streptococcus. Streptococcus shares as an etiological factor of chronic tonsillitis in children 30%, in adults - up to 15%. Less commonly, streptococcal serogroups C and J.

An important factor and development of chronic tonsillitis is the predisposition to this disease in families, which are noted for a higher incidence of streptococcus and the prevalence of chronic tonsillitis than in the population. The importance of streptococcal infection in the development of chronic tonsillitis is stricken with the fact that it is this infection that often causes the emergence of conjugated common diseases, among which rheumatism with damage to the heart and joints, glomerulonephritis and many others are considered to be the most common. In this regard, the 10th International Classification of Diseases is allocated "Streptococcal tonsillitis" (code for ICD-10 - J03.0).

Often found in chronic tonsillitis, staphylococcus should be considered as concomitant infection, but not as an etiologic factor and the development of focal infection. In chronic tonsillitis, both obligate anaerobic microorganisms, as well as intracellular and membrane parasites are found: chlamydia and mycoplasmas, which can sometimes take part in the formation of chronic tonsillitis in the form of microbial associations with "traditional" pathogens.

The involvement of viruses in the development of chronic tonsillitis is determined by the fact that under their influence, the metabolism of cells is restructured, specific enzymes, nucleic acids and protein components of the virus are synthesized, in which the protective barrier disintegrates and the path opens for the penetration of the bacterial flora that forms the focus of chronic inflammation. Thus, viruses are not the direct cause of inflammation of the tonsils, they weaken antimicrobial protection, and inflammation

The most common causes of chronic tonsillitis are adenoviruses, influenza and parainfluenza viruses, Epstein-Barr virus, herpes virus, zeneroviruses I, II and V serotypes. In early childhood, viral infection is observed more often - up to 4-6 times a year.

In most cases, the onset of chronic tonsillitis is associated with one or more tonsillitis, after which chronic inflammation and palatine tonsils occur. Conditionally pathogenic transient microflora, vegetating on the mucous membrane, including in the crypts of the tonsils, is activated during the angina, its virulence increases, and it penetrates the parenchyma of the amygdala, causing an infectious and inflammatory process. In this case, oppression of both specific and non-specific factors of the natural resistance of the macroorganism occurs. The local blood circulation is broken, the permeability of the vascular wall is increased, the level of neutrophils, phagocytic cells decreases, local immunosuppression is manifested, and as a result, the transitory microflora is activated, acute and then chronic inflammation develops.

In the formation of chronic inflammation in the tonsils, the vegetated microorganisms increase their virulence and aggressiveness by the production of exo- and zondotoxins, thereby causing toxic-allergic reactions. The microflora with chronic tonsillitis penetrates deeply into the parenchyma of the tonsils, lymphatic and blood vessels. With the help of auto radiography it was established that in case of toxic-allergic form of chronic tonsillitis the living and multiplying microflora penetrates into the parenchyma of the tonsils, into the walls and lumen of the vessels. These pathogenetic characteristics explain the patterns of common toxic-allergic reactions and associated with chronic tonsillitis diseases.

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

Pathogenesis of chronic tonsillitis

Chronic tonsillitis is a classic example of focal infection, which is based on the development of an infectious agent in the palatine tonsils and the reaction to it and the distant organs and systems of the body. It should be taken into account that the palatine tonsils do not have isolated functions peculiar only to them, they only participate in the lympho-epithelial system along with other numerous identical lymphatic formations of the body. From these positions, knowing the main patterns of the pathogenesis of chronic tonsillitis, it is easy to understand the formation of the main manifestation of the disease.

The pathogenesis of focal infection in tonsils is considered in three directions: localization of the focus, the nature of infection and inflammation and defense mechanisms. One of the explanations for the exceptional activity of metastasis of infection from a chronic tonsillar focus (in comparison with other localizations of focal infection) is the presence of wide lymphatic connections of the tonsils with the basic organs of life-support, which directly infectious, toxic, immunoactive, metabolic and other pathogenic products from the focus of infection. In the pathogenesis of chronic tonsillitis, lymphatic connections with the heart area are especially important, their presence is established in anatomical and pathophysiological studies. This can also be confirmed by embryological data on the proximity of the heart and pharyngeal pockets in the embryo. This sheds light on the understanding of the mechanism of the appearance of tonsillo-cardial connections in the formation of pathology.

Very important for understanding the pathology of lymphatic connections of the tonsils and brain centers: the pituitary gland, the ganglion of the vagus nerve and the autonomic nervous system, which is confirmed in experimental studies. In clinical practice, it is well known that after exacerbation of chronic tonsillitis, there are often changes in the innervation of the heart, and violations of extracardiac regulation are often observed outside the exacerbation in the focus of infection. Such functional disorders create prerequisites for deeper organic damage to the heart due to exposure to pathogenic agents of streptococcus or other components from the focus of infection in the tonsils.

Comparison with other localizations of chronic focal infection shows that there are no more microflora in the body, similar to chronic tonsillitis in latitude and a multiplicity of anatomic connections with life support organs and according to the conditions of chronic "incubation" of microflora. Well-known chronic foci of infection in the teeth, temporal bones, internal organs have a certain severity of the course, but such a spread of infection does not cause the body.

It is of interest to spread the pathological process to organs that do not have direct lymphogenous connections to the tonsils, for example, to the kidneys. The frequency of tonsillo-renal complications is hundreds of times less than cardiac or rheumatic. However, in this case, some of the pathogenesis inherent in lesions with direct lymphogenous connections are characteristic. In particular, in experiments on dogs, it has been shown that the onset of inflammation in the tonsils (both infectious and non-infectious) is accompanied by changes in both the heart and kidneys, where the effective blood flow is impaired (slowed down) to varying degrees. The similarity is also observed in the fact that the recurrences of acute inflammation in the tonsils are accompanied by functional impairments in the kidneys in the form of a slowing of the blood flow: this creates the conditions for the appearance of nephritic syndrome - inflammation of the renal glomeruli. Studies of renal blood flow through intramuscular injection in patients with chronic tosillitis, especially after regular angina, revealed tonsilental functional disorders.

An important link in the pathogenesis of chronic tonsillitis (closely related to the localization of the focus of infection) is the peculiar patterns of chronic inflammation in the tonsillar focus with the participation of beta-hemolytic streptococcus, which is characterized by an unusual, not characteristic for other microorganisms, aggression in the body.

A distinctive feature of chronic inflammation in comparison with acute inflammation is considered to be the duration of its course, not limited to a certain period of time. Unlike acute, chronic inflammation has no staging, and the boundary separating the acute process from chronic is fuzzy and determined by a characteristic such as a reduction in the severity of inflammation. The last stage - recovery - does not occur. The reason for this incompleteness of acute inflammation is the insufficiency (weakness) of manifestations in the focus of inflammation of protective properties. Chronic focal inflammation becomes a source of constant spreading of infectious, toxic and metabolic products into the regional and general bloodstream, which causes a general reaction and turns the local process into a common disease.

The next feature of tonsillar focal infection is the properties of the microflora of the focus, which play a decisive role in intoxication and the formation of a toxic-allergic reaction in the body, which ultimately determines the nature and severity of complications of chronic tonsillitis. Among all the microorganisms found in the tonsils in chronic tonsillitis and vegetating in crypts, only beta-hemolytic and to some extent greening streptococci are able to form a foci of infection aggressive towards distant organs, beta-hemolytic streptococcus and its vital activity to individual organs : the heart, joints, cerebral membranes and are closely related to the entire immunological system of the body. Another microflora in the crypts of the tonsils is considered as concomitant.

In the pathogenesis of chronic tonsillitis, an important role is played by violations of the protective mechanism of delimiting the focus of inflammation. The essence of the barrier function is the local suppression of the pathogens of infection and the delimitation of the focus of infection by a protective cell-vascular shaft. This protective property is lost when consecutive repetitions of acute inflammation, a decrease in the reactivity of the organism, aggressive infection, etc. When the barrier function is partially or completely lost, the inflammatory focus turns into an entrance gate for infection, and then the damage to specific organs and systems is determined by the reactive properties of the whole organism and individual organs and systems. In these conditions, tonsillar complications occur more often with exacerbations of chronic tonsillitis, although they may occur in the period between exacerbations in the focus of inflammation.

Speaking about the pathogenesis of chronic tonsillitis, it is also important to note that the natural role of palatine tonsils in the formation of immunity is completely distorted, as in the case of chronic inflammation in tonsils, new antigens are formed under the influence of pathological protein complexes (virulent microbes, endo- and exotoxins, tissue and microbial destruction products cells, etc.), which causes the formation of autoantibodies against their own tissues.

Pathological anatomy

Morphological changes of palatine tonsils in chronic tonsillitis are as diverse as its pathogenetic mechanisms, and are in direct correlation with the latter. The main pathoanatomical macro-symptom of chronic tonsillitis is the so-called solid hypertrophy, caused by the development in infected tonsils between their lobules of connective tissue, so they appear to the touch with dense, welded scars with surrounding tissues that can not be "dislocated" from their niches. From "hard" hypertrophy, "soft" hypertrophy should be distinguished when the palatine tonsils are enlarged, but they do not have inflammatory changes, and the observed hypertrophy refers to the normogenetic state that provides numerous physiological and immune functions of the tonsils. However, chronic tonsillitis can also occur atrophy of palatine tonsils caused by toxigenic inhibition or complete disappearance of the regeneration process of its parenchyma, which is replaced by sclerosis and scarring in loci of dying follicles and granules. As noted by BS Preobrazhensky (1963), the size of the tonsils is not an absolute sign of chronic tonsillitis, since an increase in their size can be observed in a number of cases, especially in children with lymphatic-hypoplastic diathesis.

Pathomorphological changes of palatine tonsils in chronic tonsillitis develop gradually and most often begin with their superficially located tissues, in contact with external pathogenic factors. However, undoubtedly, the structure and depth of lacunae play a decisive contributing factor in the development of pathoanatomical changes in the palatine tonsils, especially their excessive branching in the amygdala parenchyma. In some cases, the lacunae are particularly deep, reaching the capsules of the tonsils. In these cases, scar tissue in the peritonsillar region, which disrupts the blood supply of the tonsils and lymph drainage out of them, especially intensifies the inflammatory process that occurs in them, is especially intensive.

An important clinico-diagnostic significance is the pathoanatomical classification of the morphological changes occurring in the tonsils of the tonsils in chronic tonsillitis, given by BS Preobrazhensky (1963), which can serve as an example of the didactic technique in mastering by young specialists the organic bases of various forms of chronic tonsillitis.

According to this classification, chronic tonsillitis can occur in the following forms:

1. lacunary or cryptogenic chronic tonsillitis, characterized by chronic inflammation of the mucosa of lacunae and adjacent parenchyma; is a sign of Zach;
2. chronic parenchymal tonsillitis, in which the main changes develop in the parenchyma of the amygdala with the formation of small or larger abscesses that subsequently transform into scar tissue. Sometimes in chronic tonsillitis in the thickness of the amygdala develops a chronic abscess, which is, as a rule, filled with pus and caseous masses crypt with obliterated exit on the surface of the amygdala - intratonsillar abscess;
3. lacunar-parenchymal (total) chronic tonsillitis is observed with equal pathomorphological manifestations of the forms "a" and "b"; it should be noted that most often the chronic tonsillitis begins with the lacunar process, which then goes over to the parenchyma of the tonsils, and therefore the total defeat of the tonsils is always completed in form 3, which in pathogenetic and pathomorphological terms takes the form of a sponge, the stroma of which is made up of connective tissue, and the contents - pus, detritus , caseous, the bodies of dead and active microorganisms releasing their endo- and exotoxins to the environment;
4. chronic sclerotic tonsillitis is a special form of the pathological state of palatine tonsils, which is the last stage of the development of chronic inflammation in the amygdala parenchyma, characterized by numerous cicatricial changes in its parenchyma and capsule with numerous small and large encapsulated "cold" abscesses; as an independent form, which has nothing in common with chronic tonsillitis, sclerosing atrophy of palatine tonsils is observed in old age as one of the involutional age manifestations of lymphadenoid tissue in the body; it is characterized by the replacement of the amygdala parenchyma with a connective tissue, a significant decrease in size until the complete disappearance of palatine tonsils, general atrophy of the pharyngeal mucosa and a number of features described above.

This can be supplemented with some information on how the pathoanatomical forms of chronic tonsillitis described above can progress and what are some clinical manifestations of the changes that occur. Thus, when cryptic port is blocked in cryptogenic chronic tonsillitis, no significant general and local disturbances are observed. This form of tonsillitis is very common. The only complaints of patients with this form are putrid odor from the mouth and periodically arising abscesses in the tonsils during congestion of caseous masses in the lacunae. There may be mild hoarseness or monochorditis on the side of more pronounced pathologoanatomical manifestations of chronic cryptogenic caseous amygdalitis. After the removal of the caseous masses from the stagnant crypt, the above symptoms completely disappear until a new accumulation of these masses. With this form of chronic tonsillitis usually limited to non-operative or "semi-surgical" treatment. However, it is this form of chronic tonsillitis that is often complicated by the appearance of retentional amygdala cysts that arise in the depth of the crypt isolated from the pharynx by the fibrous diaphragm. These cysts increase in size in the crypt of detritus (from rice grain to hazelnut), reach the surface of the amygdala in the form of a smooth globular formation, covered with a shiny mucosa of a whitish-blue color. Such a cyst (usually single) can persist for years without causing the "owner" special concerns. Over time, the contents of the retentional amygdala cyst are dehydrated and impregnated with calcium salts and, slowly increasing to the size of the hazelnut and more, it is transformed into an amygdala stone, palpable as a dense foreign body. Having reached the surface of the mucous membrane, this calcite ulcerates it and falls into the pharyngeal cavity.

Chronic parenchymal tonsillitis is characterized by periodic exacerbations taking place in the form of acute viral, microbial or phlegmonous angina. The same form, reaching the state of decompensated chronic tonsillitis, often plays the role of focal infection in various metatonsillar complications.