Causes and pathogenesis of chronic tonsillitis

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

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

Causes of chronic tonsillitis

In the palatine tonsils, the infection comes into contact with immunocompetent cells that produce antibodies. The lymphoid tissue is penetrated by numerous crevices - crypts, the walls of which are covered with 3-4 layers of epithelium, in many places the epithelium is absent in islands (areas of the so-called physiological angulation). Through these de-epithelialized islands, microorganisms penetrate to the crypts and contact the tonsil cells. Each palatine tonsil contains 18-20 crypts that penetrate its parenchyma and, in addition, branch out in a tree-like manner. The surface area of the walls of all the crypts is enormous: about 300 cm ² (the area of the pharynx, for example, is 90 cm ² ). Microflora from the mouth and pharynx penetrates into the crypts, and lymphocytes from the parenchyma of the tonsils. Microorganisms enter the tonsil not only through de-epithelialized islets, but also through the epithelium of the crypt walls, forming a limited, so-called physiological, inflammation in the parietal region. Living microorganisms, their dead bodies and toxins are antigens that stimulate the formation of antibodies. Thus, in the walls of the crypts and lymphoid tissue of the tonsil (along with the entire mass of the immune system), normal immune mechanisms are formed. These processes are most active in childhood and adolescence. The body's immune system normally maintains the activity of physiological inflammation in the tonsils at a level no more than sufficient to form antibodies to various microbial agents entering the crypts. Due to certain local or general causes, such as hypothermia, viral and other diseases (especially repeated tonsillitis), weakening the immune system, physiological inflammation in the tonsils is activated, the virulence and aggressiveness of microbes in the crypts of the tonsils increases. Microorganisms overcome the protective immune barrier, limited physiological inflammation in the crypts becomes pathological, spreading to the parenchyma of the tonsil. Autoradiographic examination of the tonsils in a healthy person and in a patient with chronic tonsillitis confirms the formation of an infection focus during the development of the disease.

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

Beta-hemolytic streptococcus group A and viridans streptococcus play a significant role in the development of chronic tonsillitis and its complications. The share of streptococcus as an etiologic factor of chronic tonsillitis in children is 30%, in adults - up to 15%. Less frequently, streptococci of serological groups C and J are detected.

An important factor in the development of chronic tonsillitis is considered to be a predisposition to this disease in families, which have a higher frequency of carriage of streptococcus and prevalence of chronic tonsillitis than in the population. The significance of streptococcal infection in the development of chronic tonsillitis is reduced by the fact that this infection often becomes the cause of associated general diseases, among which the most common are rheumatism with damage to the heart and joints, glomerulonephritis and many others. In this regard, the 10th International Classification of Diseases distinguishes "Streptococcal tonsillitis" (code according to ICD-10 - J03.0).

Staphylococcus, which is often encountered in chronic tonsillitis, should be considered as a concomitant infection, but not as an etiologic factor in the process of focal infection development. In chronic tonsillitis, obligate anaerobic microorganisms are also detected, as well as intracellular and membrane parasites: chlamydia and mycoplasma, which can sometimes participate 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 restructuring of cell metabolism occurs, specific enzymes, nucleic acids and protein components of the virus are synthesized, during which the protective barrier is destroyed and the path is opened for the penetration of bacterial flora, which forms a focus of chronic inflammation. Thus, viruses are not the direct cause of the development of inflammation of the tonsils, they weaken the antimicrobial protection, and inflammation< occurs under the influence of microbial flora.

The most common causes of chronic tonsillitis are adenoviruses, influenza and parainfluenza viruses, Epstein-Barr virus, herpes virus, enteroviruses of serotypes I, II and V. In early childhood, viral infections are 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 acute inflammation in the palatine tonsils becomes chronic. Conditionally pathogenic transient microflora, vegetating on the mucous membrane, including in the crypts of the tonsils, is activated during tonsillitis, its virulence increases, and it penetrates the parenchyma of the tonsil, causing an infectious and inflammatory process. In this case, both specific and non-specific factors of the natural resistance of the macroorganism are suppressed. Local blood circulation is impaired, the permeability of the vascular wall increases, the level of neutrophils and phagocytic cells decreases, local immunodepression occurs, and, as a result, transient microflora is activated, acute and then chronic inflammation develops.

When chronic inflammation develops in the tonsils, vegetative microorganisms increase their virulence and aggressiveness by producing exo- and endotoxins, thereby causing toxic-allergic reactions. Microflora in chronic tonsillitis penetrates deep into the parenchyma of the tonsils, lymphatic and blood vessels. Autoradiography has shown that in the toxic-allergic form of chronic tonsillitis, living and multiplying microflora penetrates into the parenchyma of the tonsil, into the walls and lumen of the vessels. These pathogenetic characteristics explain the patterns of occurrence of common toxic-allergic reactions and diseases associated with chronic tonsillitis.

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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 reactions to it in distant organs and systems of the body. It is necessary to take into account that the palatine tonsils do not have isolated functions peculiar only to them, they only participate in the work of the lymph-epithelial system along with other numerous identical lymphatic formations of the body. From this position, knowing the basic patterns of pathogenesis of chronic tonsillitis, it is easy to understand the formation of the main manifestations of the disease.

The pathogenesis of focal infection in the 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 infection metastasis from a chronic tonsillar focus (compared to other localizations of focal infection) is the presence of wide lymphatic connections of the tonsils with the main organs of life support, through which infectious, toxic, immunoactive, metabolic and other pathogenic products from the focus of infection are directly distributed. In the pathogenesis of chronic tonsillitis, lymphatic connections with the heart region are especially important; their presence has been established in anatomical and pathophysiological studies. This can also be confirmed by embryological data on the proximity of the heart and pharynx rudiments in the embryo. This sheds light on the understanding of the mechanism of the emergence of tonsillocardial connections in the formation of pathology.

The lymphatic connections of the tonsils and brain centers are very important for understanding the pathology: the pituitary gland, the ganglia of the vagus nerve and the autonomic nervous system, which is confirmed in experimental studies. In clinical practice, it is well known that after an exacerbation of chronic tonsillitis, changes in the innervation of the heart often occur, and disorders of extracardiac regulation are often observed outside of an exacerbation in the focus of infection. Such functional disorders create prerequisites for deeper organic damage to the heart due to the impact of 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 other similar to chronic tonsillitis in terms of the breadth and number of anatomical connections with vital organs and in terms of chronic "incubation" of microflora in the body. Well-known chronic foci of infection in the teeth, temporal bones, internal organs have a known severity of the course, but do not cause such a spread of infection throughout the body.

Of interest is the spread of the pathological process to organs that do not have direct lymphatic connections with the tonsils, such as the kidneys. The frequency of tonsillorenal complications is hundreds of times lower than cardiac or rheumatic complications in general. However, even in this case, some pathogenesis patterns are characteristic of lesions with direct lymphatic connections. In particular, experiments on dogs have shown that the occurrence of inflammation in the tonsils (both infectious and non-infectious) is accompanied by changes in both the heart and the kidneys, where effective blood flow is impaired (slowed down) to varying degrees. At the same time, similarities are observed in that recurrences of acute inflammation in the tonsils are accompanied by functional disorders in the kidneys in the form of slowing down of blood flow: this creates conditions for the appearance of nephritic syndrome - inflammation of the renal glomeruli. Studies of renal blood flow by intramuscular administration in patients with chronic tonsillitis, especially after subsequent tonsillitis, made it possible to identify tonsillogenic functional disorders.

An important link in the pathogenesis of chronic tonsillitis (closely related to the localization of the infection site) is considered to be the peculiar patterns of chronic inflammation in the tonsillar site with the participation of beta-hemolytic streptococcus, which is distinguished by exceptional aggression in the body, which is not characteristic of other microorganisms.

A distinctive feature of chronic inflammation compared to acute inflammation is the duration of its course, which is not limited to a certain period of time. Unlike acute inflammation, chronic inflammation does not have stages, and the boundary separating the acute process from the chronic is unclear and is determined by such a characteristic as a decrease in the severity of inflammation. In this case, the last stage - recovery - does not occur. The reason for such incompleteness of acute inflammation is considered to be the insufficiency (weakness) of manifestations in the focus of inflammation of protective properties. Chronic focal inflammation becomes a source of constant spread of infectious, toxic and metabolic products into the regional and general bloodstream, which causes a general reaction and turns the local process into a general disease.

The next feature of tonsillar focal infection is considered to be 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 the crypts, only beta-hemolytic and to some extent greening streptococci are capable of forming an aggressive focus of infection in relation to distant organs, beta-hemolytic streptococcus and the products of its vital activity are tropic to individual organs: the heart, joints, meninges and are closely associated with the entire immunological system of the body. Other microflora in the crypts of the tonsils is considered concomitant.

In the pathogenesis of chronic tonsillitis, a significant role is played by violations of the protective mechanism of limiting the inflammation focus. The essence of the barrier function is the local suppression of infectious agents and limitation of the infection focus by a protective cellular-vascular shaft. This protective property is lost with successive repetitions of acute inflammation, decreased reactivity of the body, aggressive infection, etc. When the barrier function is partially or completely lost, the inflammation focus turns into an entry gate for infection, and then the damage to specific organs and systems is determined by the reactive properties of the whole body and individual organs and systems. Under these conditions, tonsillar complications occur more often during exacerbations of chronic tonsillitis, although they can also occur in the period between exacerbations in the inflammation focus.

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

Pathological anatomy

Morphological changes in the palatine tonsils in chronic tonsillitis are as diverse as its pathogenetic mechanisms, and are in direct correlation with the latter. The main pathological anatomical macro-sign of chronic tonsillitis is the so-called hard hypertrophy, caused by the development of connective tissue between the lobes of the infected tonsils, so they feel like dense, fused scars with the surrounding tissues, which cannot be “dislocated” from their niches. “Soft” hypertrophy should be distinguished from “hard” hypertrophy, when the palatine tonsils are enlarged, but there are no inflammatory changes in them, and the observed hypertrophy refers to the normogenetic state, providing numerous physiological and immune functions of the tonsils. However, chronic tonsillitis may also be accompanied by atrophy of the palatine tonsils, caused by toxic suppression or complete disappearance of the regenerative process of its parenchyma, which is replaced by sclerosis and scarring in the loci of dying follicles and granules. As noted by B.S. Preobrazhensky (1963), the size of the palatine tonsils is not an absolute sign of chronic tonsillitis, since an increase in their size may be observed in a number of cases, especially in children with lymphatico-hypoplastic diathesis.

Pathological changes in the palatine tonsils in chronic tonsillitis develop gradually and most often begin with their superficial tissues that come into contact with external pathogenic factors. However, undoubtedly, the decisive contributing factor in the development of pathological changes in the palatine tonsils is the structure and depth of the lacunae, especially their excessive branching in the parenchyma of the tonsil. In some cases, the lacunae are especially deep, reaching the capsule of the tonsil. In these cases, scar tissue in the peritonsillar region develops especially intensively, which disrupts the blood supply to the tonsils and the lymph outflow from them, thereby aggravating the inflammatory process occurring in them.

Of great clinical and diagnostic significance is the pathological classification of morphological changes occurring in the palatine tonsils in chronic tonsillitis, given by B.S. Preobrazhensky (1963), which can serve as an example of a didactic technique in the development of the organic basis of various forms of chronic tonsillitis by young specialists.

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

1. lacunar or cryptogenic chronic tonsillitis, characterized by chronic inflammation of the mucous membrane of the lacunae and adjacent parenchyma; manifested by Zach's sign;
2. chronic parenchymatous tonsillitis, in which the main changes develop in the parenchyma of the tonsil with the formation of small or larger abscesses, which subsequently transform into scar tissue. Sometimes, with chronic tonsillitis, a chronic abscess develops in the thickness of the tonsil, which is, as a rule, a crypt filled with pus and caseous masses with an obliterated outlet on the surface of the tonsil - an intratonsillar abscess;
3. lacunar-parenchymatous (total) chronic tonsillitis is observed with equal pathomorphological manifestations of forms "a" and "b"; it should be noted that most often chronic tonsillitis begins with a lacunar process, which then passes to the parenchyma of the tonsil, therefore form 3 always ends with a total lesion of the palatine tonsils, which in pathogenetic and pathomorphological terms takes the form of a sponge, the stroma of which is connective tissue, and the content is pus, detritus, caseosis, bodies of dead and active microorganisms that release their endo- and exotoxins into the environment;
4. Chronic sclerotic tonsillitis is a special form of pathological condition of the palatine tonsils, which is the last stage of development of chronic inflammation in the parenchyma of the tonsil, which is characterized by numerous cicatricial changes of 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 the palatine tonsils is observed in old age as one of the involutional age-related manifestations of lymphadenoid tissue in the body; it is characterized by replacement of the parenchyma of the tonsil with connective tissue, significant decrease in size until complete disappearance of the palatine tonsils, general atrophy of the mucous membrane of the pharynx and a number of signs described above.

The above can be supplemented with some information about how the above-described pathological forms of chronic tonsillitis can progress and what some clinical manifestations of the changes that arise are. Thus, when the crypt outlet is blocked in cryptogenic chronic tonsillitis, no significant general or local disorders are observed. This form of tonsillitis is very common. The only complaints of patients with this form are a putrid odor from the mouth and periodically occurring abscesses in the tonsils with stagnation of caseous masses in the lacunae. Mild hoarseness of the voice or monochorditis on the side of more pronounced pathological manifestations of chronic cryptogenic caseous tonsillitis may occur. After removal of caseous masses from the stagnant crypt, the above symptoms disappear without a trace until these masses accumulate again. With this form of chronic tonsillitis, non-surgical or "semi-surgical" treatment is usually limited to. However, it is this form of chronic tonsillitis that is often complicated by the occurrence of retention tonsil cysts, which arise in the depths of the crypt, isolated from the pharynx by a fibrous diaphragm. As detritus accumulates in the crypt, these cysts increase in size (from a grain of rice to a hazelnut), reaching the surface of the tonsil in the form of a smooth spherical formation covered with a shiny mucous membrane of a whitish-blue color. Such a cyst (usually single) can persist for years without causing any particular discomfort to the "owner". Over time, the contents of the retention tonsil cyst undergo dehydration and impregnation with calcium salts and, slowly increasing to the size of a hazelnut or more, transform into a tonsil stone, felt upon palpation as a dense foreign body. Having reached the surface of the mucous membrane, this calcification ulcerates it and falls out into the pharyngeal cavity.

Chronic parenchymatous tonsillitis is characterized by periodic exacerbations occurring in the form of acute viral, microbial or phlegmonous tonsillitis. This same form, having reached the state of decompensated chronic tonsillitis, most often plays the role of a focal infection in various metatonsillar complications.