ALLERGY

The term allergy comes from two Greek words allos - different, ergon - act. And a different, altered effect of certain substances on the body is literally translated. The term "allergy" was proposed by Pirke in 1906. Allergy is considered as one of the forms of immunity pathology, since allergy and immunity are provided by the same apparatus - the lymphoid system.

Immunological and allergic reactions are aimed at maintaining antigenic homeostasis, eliminating a foreign agent. At the same time, there are some differences between the reaction to the re-entry of the allergen into the body and the immune response to the antigen. So, allergies can be caused by such factors (cold, ultraviolet rays, ionizing radiation), the effect of which on the body is not accompanied by immune reactions. Allergic reactions proceed in stages with the indispensable destruction of blood, vessel walls, and tissue elements, which, in principle, distinguishes allergy from immunological reactivity. Allergy develops with the predominant participation of class E immunoglobulins, which are rarely involved in the mechanism of immunity formation. With the help of allergic reactions in the form of anaphylactic shock, inflammation, edema, etc., the body is released from the antigen (allergen) faster than with an immune response.

Allergy- this is an increased and perverted reactivity of the body to the action of substances of antigenic and non-antigenic origin.

Substances to which the body's reaction can be perverted or which can pervert the body's response are called allergens. Allergens have all the properties of antigens (macromolecular, predominantly proteinaceous nature, foreignness for a given organism, etc.). However, allergic reactions can be caused by substances that are not only antigenic in nature, but also substances that do not have these properties. These include many micromolecular compounds, such as drugs, simple chemicals (bromine, iodine, chromium, nickel), as well as more complex non-protein products (some microbial products, polysaccharides, etc.). These substances are called haptens.

Allergens can be a variety of substances. The number of allergens capable of causing allergic reactions are enormous. They are divided into allergens exogenous, i.e. entering the body from the external environment, and endogenous, arising in the body under the influence of damaging factors or in the complexation of its own tissues with non-antigenic foreign substances.

Among exogenous allergens, there are:

Infectious - a variety of pathogens of infectious diseases and their metabolic products (bacterial, viral, fungal, coccal forms) - which, once entering the body, increase the body's sensitivity and, if they enter again, an allergy phenomenon occurs;

not infectious(food, household, animal origin, chemical, medicinal and plant origin).

household (substances of an organic and inorganic nature - household, library dust, etc.). Household allergens are allergens of complex composition, which include dust particles (clothing, bed linen, furniture), fungi (in damp rooms), particles of domestic insects, bacteria (non-pathogenic staphylococci, etc.). The main allergenic component of house dust are mites (live, dead, their skins and excrement);

vegetable substances (for example: pollen of plants such as white bent grass, meadow timothy, meadow bluegrass, cocksfoot, meadow fescue, etc.);

substances of animal origin, for example, exfoliating epidermis, wool, fluff, dandruff, sweat particles;

blood serum;

some nutrients (strawberries, strawberries, egg white (albumin), milk, honey, etc.). Many foods can be allergens. However, most often they are fish, wheat, beans, tomatoes. Allergens can also be chemicals added to foods (antioxidants, dyes, aromatics, and other substances).

medicinal substances (sera, vaccines, antibiotics, some chemotherapy drugs). Any drug (with the exception of some components of biological fluids - sodium chloride, glucose, etc.) can lead to the development of drug allergies. Drugs or their metabolites are usually haptens;

some physical and chemical factors (synthetic detergents, pesticides, herbicides, etc.).

To allergens endogenous origin include autoallergens.

Autoallergens- are called tissues, cells, or proteins of the body, on which autoantibodies or sensitized lymphocytes are formed in this body and the autoallergic process develops.

Autoallergens can be formed from the body's own proteins as a result of exposure to cold, high temperature, ionizing radiation, or when microbes attach to them.

All autoallergens can be divided into 2 groups: natural (primary) and acquired (secondary).

Natural autoallergens - these are allergens that are already present in the body, these include some proteins of normal tissues (the main protein), tissues of the lens of the eye, testicles, thyroid gland, gray matter of the brain. Under normal conditions, these proteins are well isolated from immunologically competent cells and therefore they do not cause an autoallergic process. However, when these tissues are damaged, for example, during trauma, inflammation, the isolation is broken, immunologically competent cells come into contact with these proteins, and an autoallergic process can develop.

Acquired autoallergens - by origin they can be divided into two subgroups: non-infectious and infectious. The subgroup of non-infectious autoallergens includes protein denaturation products. It has been established that blood and tissue proteins in various pathological conditions acquire properties alien to the body and become autoallergens. They are found in burns and radiation sickness, in dystrophy. In all these cases, changes occur with proteins that make them foreign to the body. So the antigenic properties of whey proteins can be changed by attaching iodine to their molecule. nitro or diazo groups, and antibodies can be formed against such altered proteins.

The subgroup of infectious autoallergens includes substances formed as a result of the combination of microbial toxins and other products of infectious origin that have entered the body with cells and tissue proteins. Such complex autoallergens can, for example, be formed when some components of streptococcus are combined with myocardial connective tissue proteins. The same subgroup includes intermediate autoallergens. They are formed during the interaction of viruses with tissue cells and differ from both the virus and the tissue.

Predisposing factors in the occurrence of allergies are:

frequent vaccinations

uncontrolled intake of drugs

taking improperly stored medicines

contributing factor in the occurrence of allergies is frequent contact with chemicals.

Allergens enter the body in various ways: enterally, parenterally, through the respiratory tract, after application to the skin, mucous membranes (easier through damaged ones), transplacentally, through general and local effects of physical factors.

The mechanism of development of allergies

There are cellular and humoral mechanisms of allergic reactions. They are interconnected and considered in inseparable unity. Allergic antibodies are formed in some cells, which are then released from them and accumulate in the blood and other body fluids (humoral factors). Antibodies act through cells - sources of chemicals that have a toxic effect. These are mediators, or mediators, of allergic damage to organs and tissues. So, some cells create the basis for allergies, producing specific antibodies - reagins; others are the active link, they are called allergy effector cells.

Within the T-lymphocyte system, there are T-lymphocytes that help certain B-lymphocyte clones to produce specific antibodies to allergens. These are T-cells - helpers. In addition to them, there are also cells that provide delayed-type allergic reactions - T-lymphocytes - effectors, as well as T-lymphocytes - suppressors that suppress allergic reactions. Allergic antibodies, including reagins, are formed by descendants of B-lymphocytes - plasma cells. B-lymphocytes are involved in the formation of antibodies only with appropriate support from T-lymphocytes - helpers. In the process of formation of antibodies, another cell is involved - this is a macrophage. The main function of macrophages is to maintain the constancy of the internal environment of the body, its homeostasis. For the absorption and digestion of foreign substances in the macrophage, there is a special apparatus consisting of vacuoles, vesicles filled with highly active enzymes that break down proteins, fats, carbohydrates and nucleic acids.

Allergens of protein nature, entering the body, are filtered through macrophages. In the lysosomes of macrophages, more or less complete cleavage of allergens occurs. With their complete decay, the antigen loses its ability to cause the formation of antibodies and immunological tolerance develops to it. Partially cleaved allergen from lysosomes again "floats" to the surface of the outer membrane of the macrophage. There is evidence that it "takes" informational ribonucleic acid (and RNA) from the cell and thereby acquires even greater immunogenicity. Such a modified allergen comes into contact with the membrane receptors of a certain clone of lymphocytes and causes the formation of specific antibodies in them. The first portions of the formed antibodies, in turn, automatically increase the production of the following portions of antibodies. Normally, after passing through the stage, during which the amount of antibodies sufficient to protect the body has time to accumulate, the synthesis of antibodies automatically stops. A negative feedback is triggered, which protects against an excess of antibodies and the associated undesirable consequences - from tissue sensitization to the allergen. In organisms with an allergic constitution, this regulatory mechanism does not work clearly. An excess of antibodies accumulates in the body, which subsequently cause sensitization and tissue damage.

An immediate type of allergy is caused by sensitizing antibodies. Sensitizing antibodies are called reagins. They differ from other classes of antibodies in their chemical structure. Immunoglobulin E (reagins) is contained in the blood in a negligible amount and is quickly destroyed and completely removed from the blood after 5-6 days. Most readily they are fixed on skin cells, smooth muscles, mucous epithelium, mast cells, leukocytes, blood platelets, nerve cells. Reagins are bivalent. At one end, they are connected to the cells of the skin or internal organs, and at the other, to the determinant group of a drug or other allergen.

Cells that form allergic antibodies are not distributed diffusely throughout the organs of immunity, but are most concentrated in the tonsils, bronchial and retroperitoneal lymph nodes.

In the development of allergies, the following stages can be distinguished:

stage of immune reactions

stage of pathochemical disorders

stage of pathophysiological disorders

Stage of immune reactions: This stage is characterized by the accumulation in the body of antibodies specific for this allergen. The allergen, entering the body, is fixed in the cells of the reticuloendothelial system and causes plasmatization of lymphoid cells, in which the formation of antibodies begins. Allergic antibodies have a high degree of specificity, ie. connect only with the allergen that caused their formation. Sensitizing antibodies are called reagins. Reagins are bivalent, at one end they connect to the cells of the skin or internal organs, and at the other they attach the determinant group of a drug or other allergen. Class E antibodies and immune lymphocytes almost do not circulate in the blood, but go into the tissues and are fixed on the cells, increase sensitivity, i.e. sensitize (sensibilis - sensitive) tissues of the body to the repeated introduction (hit) of the allergen. This ends the first stage of the onset of allergies - the stage of immune reactions.

Stage 2 - pathochemical disorders. When an allergen enters the body again, antibodies class. E (reagins) react with the allergen on the surface of a wide variety of cells, even nerve cells, and damage them. Being fixed in the tissues, this complex causes a number of changes in metabolism, and first of all, the amount of oxygen absorbed by the tissues changes (initially increases, and then decreases). Under the influence of the allergen-antibody complex, tissue and cellular proteolytic and lipolytic enzymes are activated, which leads to dysfunction of the corresponding cells. As a result, a number of biologically active substances are released from the cells: histamine, serotonin, bradykinin, a slowly reacting substance of anaphylaxis (MRS-A).

In humans and animals, histamine is found in mast cells of the connective tissue, blood basophils, to a lesser extent - in neutrophilic leukocytes, platelets, smooth and striated muscles, liver cells, epithelium of the gastrointestinal tract. The participation of histamine is expressed in the fact that it causes spasm of smooth muscles and increases the permeability of blood capillaries, causing edema, urticaria, petechiae, has an exciting effect on the nerve centers, which is then replaced by depression. It irritates the nerve endings of the skin and causes itching. Histamine increases the hydrophilicity of loose connective tissue fibers, contributing to the binding of water in the tissues and the occurrence of extensive Quincke-type edema.

Serotonin is found in almost all tissues of the body, but it is especially abundant in connective tissue mast cells, spleen cells, platelets, pancreas, and in some nerve cells. It has less effect on the smooth muscles of the bronchi and bronchioles, but it causes a strong spasm of arterioles (small arteries) and a violation of blood circulation.

Bradykinin causes a sharp spasm of the smooth muscles of the intestines and uterus, to a lesser extent of the bronchi, expands the blood capillaries, increases their permeability, lowers the tone of the arterioles and causes hypotension.

"MPC - A" - it easily binds to the lipids of the cell membrane and disrupts its permeability to ions. First of all, the intake of calcium ions into the cell suffers, and it loses its ability to relax. Therefore, with the accumulation of MRS-A, spasms occur. If, under the influence of histamine, bronchospasm develops after a few seconds or minutes, then under the influence of MRS-A, the same spasm of bronchioles develops gradually, but lasts for hours.

This completes the second stage of pathochemical disorders.

Stage 3 - pathophysiological disorders. The pathophysiological stage of allergic reactions is the final expression of those immune and pathochemical processes that took place after the introduction of a specific allergen into the sensitized organism. It consists of the reaction of allergen-damaged cells, tissues, organs and the body as a whole.

Allergic damage to individual cells has been well studied on the example of erythrocytes, platelets, blood leukocytes, connective tissue cells - histiocytes, mast cells, etc. Damage also extends to nerve and smooth muscle cells, heart muscle, etc.

The response of each of the damaged cells is determined by its physiological characteristics.

So, in the nerve cell, an electrical damage potential arises, in the myofibrils of smooth muscles, erythrocytes undergo hemolysis. Damage to leukocytes is expressed in the redistribution of glycogen in the protoplasm, in lysis. Granular cells swell and throw out their granules - cell degranulation occurs. The latter process is especially pronounced in blood basophils and mast cells of loose connective tissue, the granules of which are especially rich in various biologically active substances that are mediators of allergic reactions.

Allergic damage to tissues and organs occurs as a result of damage to the cells that make up this tissue, on the one hand, and as a result of a violation of the nervous and humoral regulation of the functions of these organs, on the other. So, the contracture of the smooth muscles of the small bronchi gives bronchospasm and a decrease in the lumen of the airways.

Expansion of blood vessels and increased capillary permeability, leading to sweating of the liquid part of the blood in the tissue and causing the occurrence of urticaria, Quincke's edema, depends both on the action of allergy mediators (histamine, serotonin) on the vessels and on the disorder of peripheral and central regulation of vascular tone. The general expression of the pathophysiological phase of allergic reactions is the reaction of the body as a whole, certain allergic diseases or allergic syndromes.

The attention of the general reader is offered a book on one of the most pressing problems of our time - allergies. Perhaps there is not a single person who has not heard this strange word. And what does it mean? Is this a disease or a normal manifestation of the body? Why and who gets allergies? Can it be cured? How to live on for a person who has an allergy? All these questions and many more are answered by the author of this book. The reader will learn about the causes of the development and exacerbation of allergies, a variety of methods of treatment and prevention of this condition.

Types of allergic reactions

Depending on the time of occurrence, all allergic reactions can be divided into 2 large groups: if allergic reactions between the allergen and body tissues occur immediately, then they are called immediate-type reactions, and if after a few hours or even days, then these are delayed-type allergic reactions. According to the mechanism of occurrence, 4 main types of allergic reactions are distinguished.

Type I allergic reactions

The first type includes allergic reactions (hypersensitivity) of the immediate type. They are called atopic. Allergic reactions of immediate type are the most common immunological diseases. They affect approximately 15% of the population. Patients with these disorders have abnormal immune responses called atopic. Atopic disorders include bronchial asthma, allergic rhinitis and conjunctivitis, atopic dermatitis, allergic urticaria, angioedema, anaphylactic shock, and some cases of allergic lesions of the gastrointestinal tract. The mechanism of development of the atopic state is not fully understood. Numerous attempts by scientists to find out the causes of its occurrence have revealed a number of characteristics that distinguish some individuals with atopic conditions from the rest of the population. The most characteristic feature of such people is an impaired immune response. As a result of the impact of the allergen on the body, which occurs through the mucous membranes, an unusually high amount of specific allergic antibodies is synthesized - reagins, immunoglobulins E. People with allergies have a reduced content of another important group of antibodies - immunoglobulins A, which are "defenders" of the mucous membranes. Their deficiency opens access to the surface of the mucous membranes to a large number of antigens, which ultimately provokes the development of allergic reactions.

In such patients, along with atopy, the presence of dysfunction of the autonomic nervous system is also noted. This is especially true for people suffering from bronchial asthma and atopic dermatitis. There is an increased permeability of the mucous membranes. As a result of the fixation of so-called reagins on cells with biologically active substances, the process of damage to these cells increases, as well as the release of biologically active substances into the bloodstream. In turn, biologically active substances (BAS) with the help of special chemical mechanisms damage already specific organs and tissues. The so-called "shock" organs in the reaginic type of interaction are primarily the respiratory organs, intestines, and conjunctiva of the eyes. BAS reagin reactions are histamine, serotonin and a number of other substances.

In the reaginic type of allergy, there is a sharp increase in the permeability of the microvasculature. In this case, the fluid leaves the vessels, resulting in the development of edema and inflammation, local or widespread. The amount of discharge of mucous membranes increases, bronchospasm develops. All this is reflected in clinical symptoms.

Thus, the development of immediate type hypersensitivity begins with the synthesis of immunoglobulins E (proteins with antibody activity). The stimulus for the production of reaginic antibodies is exposure to the allergen through the mucous membrane. Immunoglobulin E, synthesized in response to immunization through the mucous membranes, is rapidly fixed on the surface of mast cells and basophils, located mainly in the mucous membranes. With repeated exposure to the antigen, immunoglobulin E fixed on the surfaces of mast cells is combined with the antigen. The result of this process is the destruction of mast cells and basophils and the release of biologically active substances, which, damaging tissues and organs, cause inflammation.

Type II allergic reactions

The second type of allergic reactions is called cytotoxic immune reactions. This type of allergy is characterized by the combination of allergen with cells first, and then antibodies with the allergen-cell system. With this triple connection, cell damage occurs. However, another component is involved in this process - the so-called complement system. Other antibodies are already involved in these reactions - immunoglobulins G, M, immunoglobulins E. The mechanism of damage to organs and tissues is not due to the release of biologically active substances, but due to the damaging effect of the above-named complement. This type of reaction is called cytotoxic. The “allergen-cell” complex can be either circulating in the body or “fixed”. Allergic diseases that have a second type of reaction are the so-called hemolytic anemia, immune thrombocytopenia, pulmonary-renal hereditary syndrome (Goodpasture's syndrome), pemphigus, and various other types of drug allergies.

III type of allergic reactions

The third type of allergic reactions is immunocomplex, it is also called "immune complex disease". Their main difference is that the antigen is not bound to the cell, but circulates in the blood in a free state, without being attached to tissue components. In the same place, it combines with antibodies, more often of classes G and M, forming antigen-antibody complexes. These complexes, with the participation of the complement system, are deposited on the cells of organs and tissues, damaging them. Inflammatory mediators are released from damaged cells and cause intravascular allergic inflammation with changes in surrounding tissues. The above complexes are most often deposited in the kidneys, joints and skin. Examples of diseases caused by reactions of the third type are diffuse glomerulonephritis, systemic lupus erythematosus, serum sickness, essential mixed cryoglobulinemia and prehepatogenic syndrome, manifested by signs of arthritis and urticaria and developing when infected with the hepatitis B virus. Increased vascular permeability plays a huge role in the development of immune complex diseases , which may be exacerbated by the development of an immediate hypersensitivity reaction. This reaction usually proceeds with the release of mast cell contents and basophils.

IV type of allergic reactions

Antibodies do not participate in reactions of the fourth type. They develop as a result of the interaction of lymphocytes and antigens. These reactions are called delayed reactions. Their development occurs 24-48 hours after the allergen enters the body. In these reactions, the role of antibodies is taken by lymphocytes sensitized by the intake of the allergen. Due to the special properties of their membranes, these lymphocytes bind to allergens. In this case, mediators, the so-called lymphokines, are formed and released, which have a damaging effect. Lymphocytes and other cells of the immune system accumulate around the place of entry of the allergen. Then comes necrosis (tissue necrosis under the influence of circulatory disorders) and the replacement development of connective tissue. This type of reaction underlies the development of some infectious-allergic diseases, such as contact dermatitis, neurodermatitis, and some forms of encephalitis. It plays a huge role in the development of such diseases as tuberculosis, leprosy, syphilis, in the development of transplant rejection, in the occurrence of tumors. Often, patients can combine several types of allergic reactions at once. Some scientists distinguish the fifth type of allergic reactions - mixed. So, for example, with serum sickness, allergic reactions of the first (reaginic), second (cytotoxic), and third (immunocomplex) types can develop.

As our knowledge of the immune mechanisms of tissue damage development increases, the boundaries between them (from the first to the fifth type) become more and more vague. In fact, most diseases are caused by the activation of different types of inflammatory responses that are interrelated.

Stages of allergic reactions

All allergic reactions in their development go through certain stages. As you know, getting into the body, the allergen causes sensitization, i.e. immunologically increased sensitivity to the allergen. The concept of allergy includes not only an increase in sensitivity to any allergen, but also the realization of this increased sensitivity in the form of an allergic reaction.

Initially, sensitivity to the antigen increases, and only then, if the antigen remains in the body or enters it again, does an allergic reaction develop. This process can be divided in time into two parts. The first part is preparation, increasing the body's sensitivity to an antigen, or, in other words, sensitization. The second part is the possibility of realizing this condition in the form of an allergic reaction.

Academician A.D. Ado singled out stage 3 in the development of allergic reactions of the immediate type.

I. Immunological stage. It covers all changes in the immune system that occur from the moment the allergen enters the body: the formation of antibodies and (or) sensitized lymphocytes and their combination with the allergen that has re-entered the body.

II. The pathochemical stage, or the stage of the formation of mediators. Its essence lies in the formation of biologically active substances. The stimulus for their occurrence is the combination of the allergen with antibodies or sensitized lymphocytes at the end of the immunological stage.

III. Pathophysiological stage, or stage of clinical manifestations. It is characterized by the pathogenic action of the formed mediators on the cells, organs and tissues of the body. Each of the biologically active substances has the ability to cause a number of changes in the body: dilate capillaries, lower blood pressure, cause spasm of smooth muscles (for example, bronchi), disrupt capillary permeability. As a result, a violation of the activity of the organ in which the incoming allergen met with the antibody develops. This phase is visible to both the patient and the doctor, because the clinical picture of an allergic disease develops. It depends on which way and to which organ the allergen entered and where the allergic reaction occurred, on what the allergen was, and also on its quantity.

According to the speed and intensity of the manifestation of clinical signs after the re-encounter of the antigen (allergen) with the body, allergic reactions are divided into two types. The first type of allergic reactions is immediate type hypersensitivity (HHNT), synonyms are immediate type hypersensitivity, anaphylactic type reaction, chimergic type reaction, B-dependent reactions. These reactions are characterized by the fact that antibodies in most cases circulate in body fluids and develop within a few minutes after repeated exposure to the antigen. The second type of allergic reaction is delayed-type hypersensitivity (HST), synonyms are delayed-type hypersensitivity, chimergic-type reaction, T-dependent reactions. This form of allergy is characterized by the fact that antibodies are fixed on the membrane of lymphocytes and are receptors for the latter. It is clinically detected several hours or days after the contact of the sensitized organism with the allergen.

Immediate type hypersensitivity (ITH). Allergic reactions of the immediate type proceed with the participation of antibodies formed in response to the antigenic load in circulating humoral media. Re-entry of the antigen leads to its rapid interaction with circulating antibodies, the formation of antigen-antibody complexes.

According to the nature of the interaction of antibodies and the allergen, there are three types of immediate hypersensitivity reactions:

the first type is reaginic, including anaphylactic reactions. The reinjected antigen meets with an antibody (IgE) fixed on tissue basophils. As a result of degranulation, histamine, heparin, hyaluronic acid, kallikrein, and other biologically active compounds are released and enter the bloodstream. Complement does not take part in reactions of this type. The general anaphylactic reaction is manifested by anaphylactic shock, local - by bronchial asthma, hay fever, urticaria;

the second type is cytotoxic, characterized by the fact that the antigen is adsorbed on the surface of the cell or represents some of its structure, and the antibody circulates in the blood. The resulting antigen-antibody complex in the presence of complement has a direct cytotoxic effect. In addition, activated killer immunocytes and phagocytes are involved in cytolysis. Cytolysis occurs with the introduction of large doses of antireticular cytotoxic serum. Cytotoxic reactions can be obtained in relation to any tissues of the recipient animal if it is injected with the blood serum of a donor previously immunized against them;

the third type - reactions like the Arthus phenomenon. Described by the author in 1903 in rabbits previously sensitized with horse serum after subcutaneous injection of the same antigen. Acute necrotizing inflammation of the skin develops at the injection site. The main pathogenetic mechanism is the formation of an antigen + antibody (IgG) complex with the complement of the system. The formed complex must be large - not less than 19 S (Swedberg units according to the sedimentation rate), otherwise it will not precipitate. At the same time, platelet serotonin is of great importance, which increases the permeability of the vascular wall, promotes the microprecipitation of immune complexes, their deposition in the vascular wall and other structures. At the same time, there is always a small amount of IgE in the blood, fixed on basophils and mast cells. Immune complexes attract neutrophils, phagocytize them, they secrete lysosomal enzymes, which, in turn, determine the chemotaxis of macrophages. Under the influence of hydrolytic enzymes released by phagocytic cells (pathochemical stage), damage (pathophysiological stage) of the vascular wall, loosening of the endothelium, thrombosis, hemorrhages, and sharp disturbances of microcirculation with foci of necrotization begin. Inflammation develops.

In addition to the Arthus phenomenon, a manifestation of allergic reactions of this type can be serum sickness - a symptom complex that occurs after parenteral administration of sera into the body of animals and humans for prophylactic or therapeutic purposes (anti-rabies, anti-tetanus, anti-plague and many others); immunoglobulins; transfused blood, plasma; hormones (ACTH, insulin, estrogen, etc.); some antibiotics, sulfonamides; with the bites of insects that release toxic compounds. The basis for the formation of serum sickness are immune complexes that arise in response to the primary, single entry of the antigen into the body.

The properties of the antigen and the characteristics of the reactivity of the organism affect the severity of the manifestation of serum sickness. When a foreign antigen enters the animal, three types of response are observed: 1) antibodies are not formed at all and the disease does not develop; 2) there is a pronounced formation of antibodies and immune complexes. Clinical signs appear quickly, as the antibody titer increases, they disappear; 3) weak antibody genesis, insufficient elimination of the antigen. Favorable conditions are created for the long-term persistence of immune complexes and their cytotoxic effect.

Symptoms are characterized by pronounced polymorphism. The onset of an acute clinical manifestation is often determined by a temperature increase of 1.5-2 ° C, regional or generalized lymphadenopathy, characteristic skin lesions (erythema, urticaria, edema) and joint tenderness. In more severe cases, acute glomerulonephritis, myocardial dysfunction, arrhythmia, vomiting, and diarrhea are observed.

In most cases, after 1-3 weeks, clinical signs disappear and recovery occurs.

Petechial fever of horses, characterized by multiple hemorrhages in the skin, mucous membranes of internal organs with the formation of infiltrates, can serve as a specific manifestation of allergic reactions of this kind. Allergic bronchoalveolitis is not uncommon in horses in urban settings.

General pathogenesis of allergic reactions of immediate type. Allergic reactions of immediate type, different in external manifestations, have common mechanisms of development. In the genesis of hypersensitivity, three stages are distinguished: immunological, biochemical (pathochemical) and pathophysiological.

The immunological stage begins with the first contact of the allergen with the body. The hit of the antigen stimulates macrophages, they begin to release interleukins that activate T-lymphocytes. The latter, in turn, trigger the processes of synthesis and secretion in B-lymphocytes, which turn into plasma cells. Plasma cells during the development of an allergic reaction of the first type produce mainly IgE, the second type - IgG 1,2,3, IgM, the third type - mainly IgG, IgM.

Immunoglobulins are fixed by cells on the surface of which there are corresponding receptors - on circulating basophils, mast cells of the connective tissue, platelets, smooth muscle cells, skin epithelium, etc. A period of sensitization sets in, sensitivity to repeated exposure to the same allergen increases. The maximum severity of sensitization occurs after 15-21 days, although the reaction may occur much earlier.

In the case of reinjection of the antigen to a sensitized animal, the interaction of the allergen with antibodies will occur on the surface of basophils, platelets, mast and other cells. Immune complexes are formed that change the properties of cell membranes. When an allergen binds to more than two adjacent immunoglobulin molecules, the membrane structure is disrupted, the cell is activated, and previously synthesized or newly formed allergy mediators begin to be released. Moreover, only about 30% of the biologically active substances contained there are released from the cells, since they are ejected only through the deformed section of the target cell membrane.

In the biochemical (pathochemical) stage, changes occurring on the cell membrane in the immunological phase due to the formation of immune complexes trigger a cascade of reactions, the initial stage of which is, apparently, the activation of cellular esterases. As a result, a number of allergy mediators are released and re-synthesized. Mediators have vasoactive and contractile activity, chemotactic properties, the ability to damage tissues and stimulate repair processes.

The role of individual mediators in the overall reaction of the body to repeated exposure to the allergen is as follows.

Histamine- one of the most important mediators of allergy. Its release from mast cells and basophils is carried out by secretion, which is an energy-dependent process. The energy source is ATP, which breaks down under the influence of activated adenylate cyclase. Histamine dilates capillaries, increases vascular permeability by dilating terminal arterioles and constricting postcapillary venules. It inhibits the cytotoxic and helper activity of T-lymphocytes, their proliferation, differentiation of B-cells and the synthesis of antibodies by plasma cells; activates T-suppressors, has a chemokinetic and chemotactic effect on neutrophils and eosinophils, inhibits the secretion of lysosomal enzymes by neutrophils.

Serotonin(5-hydroxytryptomine) - mediates smooth muscle contraction, increased permeability and vasospasm of the heart, brain, kidneys, lungs. Released in animals from mast cells. Unlike histamine, it does not have an anti-inflammatory effect. Activates the suppressor population of T-lymphocytes of the thymus and spleen. Under its influence, T-suppressors of the spleen migrate to the bone marrow and lymph nodes. Along with the immunosuppressive effect, serotonin can have an immunostimulating effect through the thymus. Enhances the sensitivity of mononuclear cells to various chemotaxis factors.

Bradykinin- the most active component of the kinin system. It changes the tone and permeability of blood vessels; lowers blood pressure; stimulates the secretion of mediators by leukocytes; to some extent affects the mobility of leukocytes; causes smooth muscle contraction. In asthmatic patients, bradykinin leads to bronchospasm. Many of the effects of bradykinin are due to a secondary increase in prostaglandin secretion.

Heparin- proteoglycan, which forms complexes with antithrombin, which prevent the coagulating effect of thrombin (blood clotting). It is released in allergic reactions from mast cells, where it is found in large quantities. In addition to anticoagulation, it has other functions: it participates in the reaction of cell proliferation, stimulates the migration of endothelial cells in capillaries, inhibits the action of complement, activates pino- and phagocytosis, and enhances the action of elastase.

Fragments complement- have anaphylactic (histamine-releasing) activity against mast cells, basophils, other leukocytes, increase the tone of smooth muscles. Under their influence, vascular permeability increases. Small polypeptide fragments of complement C 3a, C 4a, C 5a are synthesized upon activation of the complement system.

Fragment C 5a has a strong chemotactic activity for monocytes, neutrophils, basophils and eosinophils. It causes the release of granular enzymes and mediators, the aggregation of blood cells. Under the influence of C 5a, the smooth muscles of the trachea and lung parenchyma contract, which can be the cause of persistent spasmodic reactions in the bronchi of various animals.

The formation of anaphylatoxins - complement factors indicates a possible connection of immune complex diseases with the process of complement activation, which involves antibodies of the IgG and IgM classes, as well as with an immediate type hypersensitivity reaction, in which antibodies of the IgE and IgG 1 classes participate.

Metabolites oxygen- capable of damaging microorganisms, as well as cells of host tissues. Allergen-stimulated phagocytes intensively absorb oxygen, and already after 30-60 seconds, its highly reactive metabolites appear. Hydrogen peroxide (H 2 O 2), superoxide (O - 2), hydroxyl radical (OH -) and singlet oxygen (1 O 2) were found in neutrophils. These substances are also produced by monocytes / macrophages, eosinophils, basophils, mast cells. It has been shown that the toxicity of hydrogen peroxide, superoxide and hydroxyl radical is largely determined by the sensitivity of the target cell. The lungs are more likely than other organs to be exposed to high concentrations of oxygen metabolites. Active oxygen metabolites play an undoubted role in their damage. Alveolar macrophages, cells of the lung parenchyma and cells migrating to the focus of inflammation in the lungs are able to form oxygen metabolites, directly or indirectly increasing the cytotoxicity of leukocytes.

Under normal conditions, superoxide dismutases containing manganese, iron or copper-zinc as cofactors protect cells from oxygen metabolites. Hydrogen peroxide can be decomposed non-enzymatically by ascorbic acid or reduced glutathione.

Slow-reacting substance anaphylaxis (MRSA)- causes, unlike histamine, a slow contraction of the smooth muscles of the trachea and ileum of a guinea pig, human and monkey bronchioles, increases the permeability of skin vessels, and has a more pronounced bronchospastic effect than histamine. The action of MRSA is not removed by antihistamines. The term MPSA refers to a substance or group of substances representing sulfur-containing unsaturated fatty acids. These are in most cases metabolites of arachidonic acid. They are secreted by basophils, peritoneal alveolar and blood monocytes, mast cells, various sensitized lung structures. The release is induced by immune complexes and aggregated immunoglobulins.

Prostaglandins (PG) are unsaturated C 20 fatty acids containing a cyclopentane ring. Prostaglandins E, F, D are synthesized in body tissues. The ability to produce PG in different leukocytes is not the same. Monocytes (macrophages) form a significant amount of PG E 2 PG F 2a; neurophiles moderately produce PG E 2 ; lines of mast cells and basophils synthesize PG D 2 . The formation of prostaglandins, as well as other metabolites of arachidonic acid, changes under the influence of stimulation of the cell surface. The effect of PG on the immune system is varied. The most biologically active PG E 2 . It induces the differentiation of immature thymocytes, B-lymphocytes, precursor cells of hematopoiesis, their acquisition of the properties of mature cells, stimulates erythropoiesis. In the opposite way, it acts on mature leukocytes. PG E 2 inhibits the proliferation of T- and B-lymphocytes; chemotaxis, chemokinesis, leukocyte aggregation; cytotoxicity of natural killers and T cells; release of inflammatory mediators, monokines or lymphokines from mast cells, basophils, neutrophils, monocytes, lymphocytes. Exogenous prostaglandins have the ability to stimulate or inhibit the inflammatory process, cause fever, dilate blood vessels, increase their permeability, and cause erythema. Prostaglandins F cause severe bronchospasm. Their number during an attack of bronchial asthma increases 15 times. Prostaglandins E have the opposite effect, having a high bronchodilating activity.

The effect of prostaglandins on immunocompetent cells is dose-dependent and is realized mainly at the level of cyclic nucleotides.

In addition to these mediators, leukotrienes, thromboxanes, factors platelet activation, eosinophil chemotactic factorand etc.

The group of mediators of an immediate allergic reaction, which are included at a later stage of allergy, include trypsin, antitrypsin, hyaluronic acid, lysosomal enzymes, cationic proteins of neutrophils and macrophages, kinins, components of the complement system.

pathophysiological stage. It is a clinical manifestation of allergic reactions. Biologically active substances secreted by target cells have a synergistic effect on the structure and function of organs and tissues of the animal organism. The resulting vasomotor reactions are accompanied by blood flow disorders in the microcirculatory bed, and are reflected in the systemic circulation. Expansion of capillaries and an increase in the permeability of the histohematic barrier lead to the release of fluid beyond the walls of blood vessels, the development of serous inflammation. The defeat of the mucous membranes is accompanied by edema, hypersecretion of mucus.

The movement of blood into the peripheral bloodstream due to vasodilation leads to a drop in blood pressure.

Equally important in the genesis of allergic reactions of the immediate type is the state of smooth muscle fibers. Many mediators of allergy stimulate the contractile function of the myofibrils of the walls of the bronchi, intestines, and other hollow organs. The results of spastic contractions of non-striated muscle elements can manifest themselves in asphyxia, disorders of the motor function of the gastrointestinal tract, such as vomiting, diarrhea, acute pain from excessive contractions of the stomach and intestines.

The nervous component of the genesis of an immediate type of allergy is due to the influence of kinins (bradykinin), histamine, serotonin on neurons and their sensitive formations. Disorders of nervous activity with allergies can be manifested by fainting, a feeling of pain, burning, intolerable itching, and other signs.

The predominance of vasomotor reactions of the smooth muscle or nervous component in the mechanism of allergic reactions depends on the nature of the allergen, the ways it enters the body, the type of animal, and their individual characteristics.

Immediate-type hypersensitivity reactions end with either recovery or death, which may be caused by asphyxia or acute hypotension.

The struggle to restore disturbed homeostasis begins already at the immunological stage through the formation of immune complexes that bind the allergen; continues in the second stage due to the release of biologically active substances, the appearance of a superoxide radical and ends in the third stage by the final elimination of the allergen and the neutralization of allergy mediators.

Anaphylaxis. The most common type of immediate hypersensitivity in farm animals is anaphylaxis.

Anaphylaxis (from the Greek ana - on the contrary, philaxis - protection, protection) - a state of increased reactivity of animals to repeated parenteral ingestion of a foreign substance of a protein nature. The term was proposed by Richet in 1902. Under experimental conditions, he observed the death of dogs from repeated injections of eel serum.

In experiments on animals of various types, anaphylaxis is easily modeled by reinjection of the allergen into sensitized animals. The classic object for the study of anaphylaxis is the guinea pig (GP Sakharov, 1905). Already a few minutes after the second parenteral administration of a foreign protein (horse serum), characteristic signs develop. The animal begins to worry, ruffles its hair, often scratches its muzzle with its paw, takes a lateral position; breathing becomes difficult, intermittent, convulsive muscle contraction appears; involuntary separation of feces and urine occurs; respiratory movements slow down, and after a few minutes the animal dies with signs of asphyxia. This clinical picture is combined with a drop in blood pressure, a decrease in body temperature, acidosis, and an increase in the permeability of blood vessels. An autopsy of a guinea pig that died from anaphylactic shock reveals foci of emphysema and atelectasis in the lungs, multiple hemorrhages on the mucous membranes, and unclotting blood.

In animals of different species, anaphylaxis proceeds ambiguously. After the administration, especially intravenous, of a permissive dose of the allergen in animals, certain signs of immediate hyperergy may prevail. Moreover, a change in the functions of the so-called "shock" organs is characteristic. In a rabbit, these are the vessels of the pulmonary circulation. They react with a sharp contraction of the arterioles of the lungs, expansion of the right ventricle, hypotension. However, death is extremely rare. Dogs are more sensitive. Due to spastic contraction of the portal vein, they develop congestion of the vessels of the mesentery, develop hemorrhagic enteritis, cystitis; fecal masses and urine are stained red by erythrocytes. In horses, the “shock” organ is the skin. High mortality from anaphylaxis was noted after reinjection of anthrax vaccine in sheep and cattle. In pigs, after repeated administration of anti-erysipelas serum, after 5-6 hours, signs of anaphylaxis without a lethal outcome may appear with the restoration of normal vital activity.

The development of anaphylactic shock can be prevented by administering small doses of the antigen to the sensitized animal 1-2 hours before the injection of the required volume of the drug. Small amounts of antigen bind antibodies, and the resolving dose is not accompanied by the development of immunological and other stages of immediate hypersensitivity. The described temporary removal of hypersensitivity to the repeated introduction of the allergen is called desensitization.

atopy. Among the reactions of the first type, along with anaphylactic ones, atopy is also distinguished (from the Greek thopos - place, a - alien, unusual). Atopy is a genetically determined predisposition to pathological immune reactions in response to the action of allergens, which are harmless to most people and animals.

Currently, atonic diseases mean diseases caused by hyperproduction of IgE. Atopy is characterized by hereditary predisposition, although the mode of inheritance is not clear. In the pathogenesis of atopy, spasm of smooth muscles, increased permeability of the mucous membrane of the gastrointestinal tract and respiratory tract, venous hyperemia, and edema are especially noted. In addition, changes in the secretion of glands (dyskrinia) modulated by non-specific (vegetative) factors are found.

Atopic diseases are relatively well studied in humans (atopic bronchial asthma, atopic dermatitis, allergic rhinitis and conjunctivitis, hay fever, etc.). Atopic diseases in animals have been little studied. Nevertheless, the phenomena of hay fever with asthmatic dyspnea and bronchitis in cattle are known; in horses, a hypersensitivity reaction to plant antigens of hay and bedding has been described in the form of emphysematous bronchitis, to insect bites; Dogs and cats may develop allergic reactions to food components, milk, fish, granulated dry food, etc.

Anaphylactoid reactions. Anaphylactoid reactions (pseudo-allergic, anaphylactic) are characterized by increased reactivity of the body, not associated with immunological interactions of the antibody with the antigen, and arise as a result of the direct influence of damaging factors on target cells, followed by the release of mediators (biochemical stage) and their aftereffects (pathophysiological stage).

Anaphylactoid reactions can be caused by physical factors - heat, cold, pressure, increased physical activity, vaccines, serums, polypeptides, dextrins, muscle relaxants, waste products of helminths, etc.

They can have a direct direct damaging effect on basophils, mast and other cells with the release of allergy mediators; stimulate mast cells with polypeptides; influence the enzyme systems synthesizing prostaglandins and leukotrienes from arachidic acid with subsequent angiospastic effect; cause aggregation of blood cells. The pathophysiological stage in this case, in terms of clinical manifestations (skin itching, erythema, edema, diathesis, hypotension, bradycardia) is very similar to that in the development of immediate and tuberculin type hypersensitivity in sensitized recipients.

In veterinary practice, of great interest is a para-allergy that occurs when an animal is sensitized by one type of pathogen to the introduction of an antigen of another origin - microorganisms or their toxins. It has been established, for example, that a positive reaction to tuberculin is often recorded in animals sensitized with low-virulence atypical mycobacteria carrying antigens related to tuberculosis pathogens. To identify the specificity of the sample in these cases, a complex antigen is used, which makes it possible to identify the pathogen that has sensitized the body of an animal.

Pathogenetic aspects of the development of systemic and locally manifested paraallergy in animals have not yet been sufficiently identified, but its probability must be taken into account.

Delayed type hypersensitivity (DST). Allergic reactions of the delayed or tuberculin type are characterized by the fact that, in contrast to the reactions of the immediate type, the response of the sensitized animal to the antigen does not occur immediately, but at least 24 hours after contact with the allergen.

The signs of HCHT were described by Koch at the beginning of the 19th century. He discovered that the skin of tuberculosis patients and humans is very sensitive to tuberculin, a product of mycobacteria.

This type of reaction proceeds with the predominant participation of sensitized lymphocytes, therefore it is considered as a pathology of cellular immunity. The slowdown in the reaction to the antigen is explained by the need for a longer time for the accumulation of lymphocytic cells (T- and B-lymphocytes of different populations, macrophages, basophils, mast cells) in the area of ​​​​action of a foreign substance compared to the humoral antigen + antibody reaction with immediate type hypersensitivity.

Delayed-type reactions develop with infectious diseases, vaccinations, contact allergies, autoimmune diseases, with the introduction of various antigenic substances into animals, and the application of haptens. They are widely used in veterinary medicine for allergic diagnosis of latent forms of chronic infectious diseases such as tuberculosis, glanders, and some helminthic infestations (echinococcosis).

Like any other reaction to an allergen, HPRT proceeds in three stages; their manifestation has its own specifics.

In the pathochemical stage, stimulated T-lymphocytes synthesize a large number of lymphokines - mediators of HST. They, in turn, involve cells of other types, such as monocytes / macrophages, neutrophils, in response to a foreign antigen.

The most important in the development of the pathochemical stage are the following mediators:

the migration-inhibiting factor is responsible for the presence of monocytes/macrophages in the inflammatory infiltrate; it is assigned the most important role in the formation of the phagocytic response;

factors affecting macrophage chemotaxis, their adhesion, resistance;

mediators that affect the activity of lymphocytes, such as a transfer factor that promotes the maturation of T-cells in the body of the recipient after the introduction of sensitized cells; a factor that causes blast transformation and proliferation; a suppression factor that inhibits the immune response to an antigen, etc.;

a chemotaxis factor for granulocytes that stimulates their emigration, and an inhibitory factor that acts in the opposite way;

interferon, which protects the cell from the introduction of viruses;

skin-reactive factor, under the influence of which the permeability of the skin vessels increases, swelling, redness, tissue thickening at the site of antigen reinjection appear.

The influence of allergy mediators is limited by opposing systems that protect target cells.

In the pathophysiological stage, biologically active substances released by damaged or stimulated cells determine the further development of delayed-type allergic reactions.

Local tissue changes in delayed-type reactions can be detected as early as 2-3 hours after exposure to a resolving dose of antigen. They are manifested by the initial development of a granulocytic reaction to irritation, then lymphocytes, monocytes and macrophages migrate here, accumulating around the vessels. Along with migration, cell proliferation takes place in the focus of an allergic reaction. However, the most pronounced changes are observed after 24-48 hours. These changes are characterized by hyperergic inflammation with pronounced signs.

Delayed allergic reactions are induced mainly by thymus-dependent antigens - purified and unpurified proteins, microbial cell components and exotoxins, virus antigens, low molecular weight protein-conjugated haptens. The reaction to the antigen in this type of allergy can be formed in any organ, tissue. It is not associated with the participation of the complement system. The main role in pathogenesis belongs to T-lymphocytes, which has been proven in experiments with neonatal thymectomy, which prevents the development of delayed-type hypersensitivity. The genetic control of the reaction is carried out either at the level of individual subpopulations of T- and B-lymphocytes, or at the level of intercellular relationships.

Depending on the etiological factor and localization, several types of delayed-type hypersensitivity are considered:

contact allergic reaction occurs in places of direct interaction of the allergen with the surface of the skin, mucous membranes and serous membranes. Cellular infiltrate is localized in the epidermis mainly due to mononuclear cells. The reaction is manifested by contact allergic dermatitis, photodermatosis. For the development of photoallergic reactions, two conditions are necessary: ​​the ingestion of a photosensitizer by any means (oral, oral, inhalation, through the skin), the formation of photosensitive substances in the animal's body itself and its subsequent exposure to ultraviolet rays. Some antiseptics, diuretics, antibiotics, eosin, chlorophyll, fluorescein, etc. can cause skin sensitization. Endogenous tissue substances formed during solar irradiation can also be antigens.

In cattle, sheep, horses, pigs, after eating clover, buckwheat, under the influence of ultraviolet radiation, signs of the so-called "clover" or "buckwheat" disease can be observed on unpigmented areas of the skin. It is manifested by erythema, eczematous lesions, itching, swelling, inflammation;

basophilic skin sensitivity develops in a sensitized organism with predominant infiltration by basophils. It is thymus-dependent, observed in the localization of malignant tumors, with tissue damage by helminths and mites;

hypersensitivity causing graft rejection. The reaction is cellular, with high activity of cytolytic T-lymphocytes.

An allergic reaction is a pathological response of the body's defense system to the influence of an irritant - an allergen. Ultimately, the body begins to synthesize antibodies that are designed to resist allergens, but are perceived by them as hostile.

Thus, antibodies lead not only to the neutralization of the allergen, but also to damage to healthy tissues, provoke various types of allergic reactions. Most often, allergies occur in one form or another of skin dermatosis.

Types of allergic reactions: etiological and provoking factors

The etiological factors that cause the development of different types of allergic reactions are currently not well understood. They are triggered by the earlier sensitization of the body by an allergen (one or more). An allergen is a substance to which the defense system responds with an atypical reaction. Allergens can be any antigens that the body regards as foreign.

All allergens are conditionally divided into 2 groups:

1. infectious:
. particles of bacteria;
. mushroom components;
. components of viruses;
. helminth particles.

2. Non-infectious:
. plant pollen;
. dust (street, book, house);
. detergents and cosmetics (powders, soaps, perfumes, oils, gels, shampoos);
. food products (milk, seafood, chocolate, fish, citrus fruits, honey, nuts);
. wool, skin particles, saliva of animals (mainly cats and dogs);
. chemicals (varnishes, paints, resins, solvents);
. poisons of animal origin (stings of bees, bumblebees, wasps);
. medicines (mainly antibiotics);
. latex (disposable gloves, condoms);
. ultra-violet rays;
. cold;
. synthetic clothing.

Factors provoking various types of allergic reactions

In order to trigger manifestations of an allergic reaction, in addition to exposure to an allergen, one or more provoking factors must occur that significantly increase the risk of an allergy.

The occurrence of an allergic reaction has a direct relationship with the individual susceptibility of the body. The effect of one allergen on the body of different people is different.

So, for example, one person consumes seafood without consequences, while in another they lead to the development of some type of allergic reaction.

Types of allergic reactions: classification

There are 4 types of allergic reactions:
. First type
This is an immediate reaction, which proceeds according to the anaphylactic type (Quincke's edema, anaphylactic shock, bronchial asthma, allergic rhinitis or urticaria). After exposure to an allergen, the body's response in the form of an allergy is formed after a few minutes - several hours.

. Second type
It proceeds as a cytotoxic reaction, it is based on the cytolysis (destruction) of cells. It develops more slowly, and lasts longer (up to several hours). Manifested by thrombocytopenia, hemolytic anemia, toxic allergies.

. Third type
It is called the Arthus phenomenon and proceeds according to the type of immunocomplex reaction. It is based on the formation of complexes of antibodies and allergens (antigens), which are deposited on the walls of capillaries and destroy them. This reaction continues for several days. Manifested by allergic conjunctivitis, glomerulonephritis, systemic lupus erythematosus, hemorrhagic vasculitis.

. Fourth type
It proceeds according to a delayed type of allergic reaction or late hypersensitization. Develops within at least 24 hours. Manifested by contact dermatitis, rhinitis, asthma.

Types of allergic reactions: skin manifestations

The main manifestations of skin allergic reactions include:

. atopic dermatitis- manifested by dryness, itching and irritation of the skin;

. contact dermatitis- accompanied by hyperemia, swelling, itching of the skin area in contact with the allergen, the appearance of rashes in the form of papules and vesicles;

. hives- similar to a nettle burn and is accompanied by the appearance of hyperemic spots raised above the skin surface, with a tendency to merge, intense itching, weakness, dizziness;

. eczema- manifested by a multiple rash in the form of vesicles with serous contents, prone to open and form erosion, and subsequently scabs, scars;

. toxicoderma- accompanied by a profuse rash of a pink or red hue, which later leads to the formation of blisters;

. neurodermatitis- manifested by night itching, rashes in the form of hyperemic spots, which later merge into plaques, swelling of the skin;

. angioedema- accompanied by swelling of the mucous membranes, swelling of the subcutaneous fatty tissue (more often manifested on the face), hoarseness, difficulty breathing, coughing;

. Lyell's syndrome- refers to severe drug allergy, manifested by the appearance of vesicles, which, opening up, form cracks, erosions, ulcers on the skin;

. steven johnson syndrome- proceeds according to the type of exudative erythema with the appearance of a bright red bleeding rash, the appearance of itching, swelling, fever, weakness, myalgia, headaches.
Methods for identifying types of allergic reactions

In order to confirm the diagnosis and identify a specific irritant, various tests and analyzes are performed.

. Blood tests
With the development of allergies in the peripheral blood, an increased level of eosinophils, class E immunoglobulins is detected.

. Skin tests
The patient is injected intradermally with various allergens, their number can be up to 20 varieties. Each allergen is applied to a specific skin area. A positive reaction manifests itself for half an hour in the form of redness, itching and swelling. The more intense the manifestations, the stronger the effect of the allergen for this patient.

You should stop taking antihistamines 48 hours before performing skin tests, because their use can cause false test results.

. Skin tests
Applications of paraffin, petroleum jelly and a number of allergens (chromium, benzocaine, drugs) are applied to the skin. Applications must be kept on the skin for 24 hours. They are used in the diagnosis of contact dermatitis, eczema.
. Provocative tests
It is 100% reliable in establishing the cause of allergies, but the most dangerous method of examination. Provocative tests are performed in a hospital under the supervision of a group of doctors. The alleged allergen is introduced into the digestive tract, nasopharynx, sublingually.

According to modern concepts, all allergic reactions, all manifestations of allergies depending on the rate of occurrence and intensity of manifestation of clinical signs after a repeated meeting of the allergen with the body, they are divided into two groups:

* Allergic reactions of immediate type;

* Allergic reactions of the delayed type.

Allergic reactions of immediate type (immediate type hypersensitivity, anaphylactic type reaction, chimergic type reaction, B - dependent reactions). These reactions are characterized by the fact that antibodies in most cases circulate in body fluids, and they develop within a few minutes after repeated exposure to the allergen.

Allergic reactions of the immediate type proceed with the participation of antibodies formed in response to the antigenic load in circulating humoral media. Re-entry of the antigen leads to its rapid interaction with circulating antibodies, the formation of antigen-antibody complexes. According to the nature of the interaction of antibodies and the allergen, there are three types of immediate hypersensitivity reactions: first type - r e a g i n o v y, including anaphylactic reactions. The reinjected antigen meets with an antibody (Ig E) fixed on tissue basophils. As a result of degranulation, histamine, heparin, hyaluronic acid, kallecrein, and other biologically active compounds are released and enter the bloodstream. Complement does not take part in reactions of this type. The general anaphylactic reaction is manifested by anaphylactic shock, local - by bronchial asthma, hay fever, urticaria, Quincke's edema.

Second type - cytotoxic, characterized by the fact that the antigen is sorbed on the surface of the cell or represents some of its structure, and the antibody circulates in the blood. The resulting antigen-antibody complex in the presence of complement has a direct cytotoxic effect. In addition, activated killer immunocytes and phagocytes are involved in cytolysis. Cytolysis occurs with the introduction of large doses of antireticular cytotoxic serum. Cytotoxic reactions can be obtained in relation to any tissues of the recipient animal if it is injected with the blood serum of a donor previously immunized against them.

The third type is reactions of the Artyus phenomenon type. It was described by the author in 1903 in rabbits previously sensitized with horse serum after subcutaneous injection of the same antigen. Acute necrotizing inflammation of the skin develops at the injection site. The main pathogenetic mechanism is the formation of an antigen + antibody complex (Ig G) with the complement of the system. The formed complex must be large, otherwise it does not precipitate. At the same time, platelet serotonin is of great importance, which increases the permeability of the vascular wall, promotes the microprecipitation of immune complexes, their deposition in the walls of blood vessels and other structures. At the same time, there is always a small amount (Ig E) in the blood, fixed on basophils and mast cells. Immune complexes attract neutrophils, phagocytize them, they secrete lysosomal enzymes, which, in turn, determine the chemotaxis of macrophages. Under the influence of hydrolytic enzymes released by phagocytic cells (pathochemical stage), damage (pathophysiological stage) of the vascular wall, loosening of the endothelium, thrombosis, hemorrhages, and sharp disturbances of microcirculation with foci of necrotization begin. Inflammation develops.

In addition to the Arthus phenomenon, serum sickness can serve as a manifestation of allergic reactions of this type.

Serum sickness- a symptom complex that occurs after parenteral administration of sera into the body of animals and humans for prophylactic or therapeutic purposes (anti-rabies, anti-tetanus, anti-plague, etc.); immunoglobulins; transfused blood, plasma; hormones (ACTH, insulin, estrogen, etc.) some antibiotics, sulfonamides; with the bites of insects that release toxic compounds. The basis for the formation of serum sickness are immune complexes that arise in response to the primary, single entry of the antigen into the body.

The properties of the antigen and the characteristics of the reactivity of the organism affect the severity of the manifestation of serum sickness. When a foreign antigen enters the animal, three types of response are observed: 1) antibodies are not formed at all and the disease does not develop; 2) there is a pronounced formation of antibodies and immune complexes. Clinical signs appear quickly, as the antibody titer increases, they disappear; 3) weak antibody genesis, insufficient elimination of the antigen. Favorable conditions are created for the long-term persistence of immune complexes and their cytotoxic effect.

Symptoms are characterized by pronounced polymorphism. The prodromal period is characterized by hyperemia, increased skin sensitivity, enlarged lymph nodes, acute pulmonary emphysema, damage and swelling of the joints, swelling of the mucous membranes, albuminuria, leukopenia, thrombocytopenia, increased ESR, hypoglycemia. In more severe cases, acute glomerulonephritis, myocardial dysfunction, arrhythmia, vomiting, and diarrhea are observed. In most cases, after 1-3 weeks, the clinical signs disappear and recovery occurs.

Bronchial asthma - It is characterized by a sudden attack of suffocation with a sharp difficulty in the expiratory phase as a result of a diffuse obstruction in the system of small bronchi. Manifested by bronchospasm, swelling of the mucous membrane of the bronchi, hypersecretion of the mucous glands. In the atopic form, the attack begins with a cough, then a picture of expiratory suffocation develops, a large number of dry whistling rales are heard in the lungs.

Pollinosis (hay fever, allergic rhinitis) - a recurrent disease associated with the inhalation and conjunctiva of plant pollen from the air during their flowering period. It is characterized by hereditary predisposition, seasonality (usually spring-summer, due to the flowering period of plants). It is manifested by rhinitis, conjunctivitis, irritation and itching of the eyelids, sometimes general weakness, fever. An increased amount of histamine, reagins (Ig E), eosinophilic granulocytes, globulin fraction of blood serum, an increase in transaminase activity are detected in the blood. Attacks of the disease disappear after contact with plant allergens is stopped after a few hours, sometimes after a few days. The rhino-conjunctival form of pollinosis can end with a visceral syndrome, in which a number of internal organs are affected (pneumonia, pleurisy, myocarditis, etc.).

Urticaria and angioedema- occur when exposed to plant, pollen, chemical, epidermal, serum, drug allergens, house dust, insect bites, etc. This disease usually begins suddenly, with the manifestation of very often unbearable itching. At the site of scratching, hyperemia instantly occurs, then there is a rash on the skin of itchy blisters, which are swelling of a limited area, mainly the papillary layer of the skin. There is an increase in body temperature, swelling of the joints. The illness lasts from several hours to several days.

One type of urticaria is Quincke's edema (giant urticaria, angioedema). With Quincke's edema, skin itching usually does not occur, since the process is localized in the subcutaneous layer, not spreading to the sensitive endings of the skin nerves. Sometimes urticaria and Quincke's edema proceed very rapidly, preceding the development of anaphylactic shock. In most cases, the acute phenomena of urticaria and Quincke's edema are completely cured. Chronic forms are difficult to treat, characterized by an undulating course with alternating periods of exacerbation and remission. The generalized form of urticaria is very difficult, in which edema captures the mucous membrane of the mouth, soft palate, tongue, and the tongue hardly fits in the oral cavity, while swallowing is very difficult. In the blood, an increase in the content of eosinophilic granulocytes, globulins and fibrinogen, a decrease in the level of albumins are found.

General pathogenesis of immediate allergic reactions .

Allergic reactions of immediate type, different in external manifestations, have common mechanisms of development. In the genesis of hypersensitivity, three stages are distinguished: immunological, biochemical (pathochemical) and pathophysiological. Immunological stage begins with the first contact of the allergen with the body. The hit of the antigen stimulates macrophages, they begin to release interleukins that activate T-lymphocytes. The latter, in turn, trigger the processes of synthesis and secretion in B-lymphocytes, which turn into plasma cells. Plasma cells during the development of an allergic reaction of the first type produce mainly Ig E, the second type - Ig G 1,2,3, Ig M, the third type - mainly Ig G, Ig M.

Immunoglobulins are fixed by cells on the surface of which there are corresponding receptors - on circulating basophils, mast cells of the connective tissue, platelets, smooth muscle cells, skin epithelium, etc. A period of sensitization sets in, sensitivity to repeated exposure to the same allergen increases. The maximum severity of sensitization occurs after 15-21 days, although the reaction may occur much earlier. In the case of reinjection of the antigen to a sensitized animal, the interaction of the allergen with antibodies will occur on the surface of basophils, platelets, mast and other cells. When an allergen binds to more than two adjacent immunoglobulin molecules, the membrane structure is disrupted, the cell is activated, and previously synthesized or newly formed allergy mediators begin to be released. Moreover, only about 30% of the biologically active substances contained there are released from the cells, since they are ejected only through the deformed section of the target cell membrane.

IN pathochemical stage changes occurring on the cell membrane in the immunological phase due to the formation of immune complexes trigger a cascade of reactions, the initial stage of which is, apparently, the activation of cellular esterases. As a result, a number of allergy mediators are released and re-synthesized. Mediators have vasoactive and contractile activity, chemotoxic properties, the ability to damage tissues and stimulate repair processes. The role of individual mediators in the overall reaction of the body to repeated exposure to the allergen is as follows.

Histamine - one of the most important mediators of allergy. Its release from mast cells and basophils is carried out by secretion, which is an energy-dependent process. The energy source is ATP, which breaks down under the influence of activated adenylate cyclase. Histamine dilates capillaries, increases vascular permeability by dilating terminal arterioles and constricting postcapillary venules. It inhibits the cytotoxic and helper activity of T-lymphocytes, their proliferation, differentiation of B-cells and the synthesis of antibodies by plasma cells; activates T-suppressors, has a chemokinetic and chemotactic effect on neutrophils and eosinophils, inhibits the secretion of lysosomal enzymes by neutrophils.

Serotonin - mediates smooth muscle contraction, increased permeability and vasospasm of the heart, brain, kidneys, and lungs. Released in animals from mast cells. Unlike histamine, it does not have an anti-inflammatory effect. Activates the suppressor population of T-lymphocytes of the thymus and spleen. Under its influence, T-suppressors of the spleen migrate to the bone marrow and lymph nodes. Along with the immunosuppressive effect, serotonin can have an immunostimulating effect through the thymus. Enhances the sensitivity of mononuclear cells to various chemotaxis factors.

Bradykinin - the most active component of the kinin system. It changes the tone and permeability of blood vessels; lowers blood pressure, stimulates the secretion of mediators by leukocytes; to some extent affects the mobility of leukocytes; causes smooth muscle contraction. In asthmatic patients, bradykinin leads to bronchospasm. Many of the effects of bradykinin are due to a secondary increase in prostaglandin secretion.

Heparin - proteoglycan, which forms complexes with antithrombin, which prevent the coagulating effect of thrombin (blood clotting). It is released in allergic reactions from mast cells, where it is found in large quantities. In addition to anticoagulation, it has other functions: it participates in the reaction of cell proliferation, stimulates the migration of endothelial cells into the capillaries, inhibits the action of complement, activates pino- and phagocytosis.

Complement fragments - have anaphylactic (histamine-releasing) activity against mast cells, basophils, other leukocytes, increase the tone of smooth muscles. Under their influence, vascular permeability increases.

Slowly reacting substance of anaphylaxis (MRSA) - unlike histamine, causes a slow contraction of the smooth muscles of the trachea and ileum of a guinea pig, human and monkey bronchioles, increases the permeability of skin vessels, and has a more pronounced bronchospastic effect than histamine. The action of MRSA is not removed by antihistamines. It is secreted by basophils, peritoneal alveolar and blood monocytes, mast cells, various sensitized lung structures.

Protoglandins - prostaglandins E, F, D are synthesized in body tissues. Exogenous prostaglandins have the ability to stimulate or inhibit the inflammatory process, cause fever, dilate blood vessels, increase their permeability, and cause erythema. Prostaglandins F cause severe bronchospasm. Prostaglandins E have the opposite effect, having a high bronchodilating activity.

pathophysiological stage. It is a clinical manifestation of allergic reactions. Biologically active substances secreted by target cells have a synergistic effect on the structure and function of organs and tissues of the animal organism. The resulting vasomotor reactions are accompanied by blood flow disorders in the microcirculatory bed, and are reflected in the systemic circulation. Expansion of capillaries and an increase in the permeability of the histohematic barrier lead to the release of fluid beyond the walls of blood vessels, the development of serous inflammation. The defeat of the mucous membranes is accompanied by edema, hypersecretion of mucus. Many mediators of allergy stimulate the contractile function of the myofibrils of the walls of the bronchi, intestines, and other hollow organs. The results of spastic contractions of muscle elements can manifest themselves in asphyxia, disorders of the motor function of the gastrointestinal tract, such as vomiting, diarrhea, acute pain from excessive contractions of the stomach and intestines.

The nervous component of the genesis of an immediate type of allergy is due to the influence of kinins (bradykinin), histamine, serotonin on neurons and their sensitive formations. Disorders of nervous activity with allergies can be manifested by fainting, a feeling of pain, burning, unbearable itching. Immediate-type hypersensitivity reactions end with either recovery or death, which may be caused by asphyxia or acute hypotension.

Delayed allergic reactions (hypersensitivity of the delayed type, hypersensitivity of the delayed type, T - dependent reactions). This form of allergy is characterized by the fact that antibodies are fixed on the membrane of lymphocytes and are receptors for the latter. Clinically detected 24-48 hours after the contact of the sensitized organism with the allergen. This type of reaction proceeds with the predominant participation of sensitized lymphocytes, therefore it is considered as a pathology of cellular immunity. The slowdown in the reaction to the antigen is explained by the need for a longer time for the accumulation of lymphocytic cells (T- and B - lymphocytes of different populations, macrophages, basophils, mast cells) in the area of ​​​​action of a foreign substance compared to the humoral reaction antigen + antibody with immediate type hypersensitivity. Delayed-type reactions develop with infectious diseases, vaccinations, contact allergies, autoimmune diseases, with the introduction of various antigenic substances into animals, and the application of haptens. They are widely used in veterinary medicine for allergic diagnosis of latent forms of chronic infectious diseases such as tuberculosis, glanders, and some helminthic infestations (echinococcosis). Delayed-type reactions are tuberculin and maleic allergic reactions, rejection of transplanted tissue, autoallergic reactions, bacterial allergies.

General pathogenesis of delayed-type allergic reactions

Delayed hypersensitivity occurs in three stages:

IN pathochemical stage stimulated T-lymphocytes synthesize a large number of lymphokines - mediators of HRT. They, in turn, involve other types of cells, such as monocytes / macrophages, neutrophils, in response to a foreign antigen. The most important in the development of the pathochemical stage are the following mediators:

the migration-inhibiting factor is responsible for the presence of monocytes/macrophages in the inflammatory infiltrate; it is assigned the most important role in the formation of the phagocytic response;

factors affecting macrophage chemotaxis, their adhesion, resistance;

mediators that affect the activity of lymphocytes, such as a transfer factor that promotes the maturation of T-cells in the body of the recipient after the introduction of sensitized cells; a factor that causes blast transformation and proliferation; a suppression factor that inhibits the immune response to an antigen, etc.;

a chemotaxis factor for granulocytes that stimulates their emigration, and an inhibitory factor that acts in the opposite way;

interferon, which protects the cell from the introduction of viruses;

skin-reactive factor, under the influence of which the permeability of the skin vessels increases, swelling, redness, tissue thickening at the site of antigen reinjection appear.

The influence of allergy mediators is limited by opposing systems that protect target cells.

IN pathophysiological stage biologically active substances released by damaged or stimulated cells determine the further development of delayed-type allergic reactions.

Local tissue changes in delayed-type reactions can be detected as early as 2-3 hours after exposure to a resolving dose of antigen. They are manifested by the initial development of a granulocytic reaction to irritation, then lymphocytes, monocytes and macrophages migrate here, accumulating around the vessels. Along with migration, cell proliferation takes place in the focus of an allergic reaction. However, the most pronounced changes are observed after 24-48 hours. These changes are characterized by hyperergic inflammation with pronounced signs.

Delayed allergic reactions are induced mainly by thymus-dependent antigens - purified and unpurified proteins, microbial cell components and exotoxins, virus antigens, low molecular weight protein-conjugated haptens. The reaction to the antigen in this type of allergy can be formed in any organ, tissue. It is not associated with the participation of the complement system. The main role in pathogenesis belongs to T-lymphocytes. The genetic control of the reaction is carried out either at the level of individual subpopulations of T- and B-lymphocytes, or at the level of intercellular relationships.

malleic allergic reaction used to detect glanders in horses. The application of purified mallein obtained from pathogens to the mucous membrane of the eye of infected animals after 24 hours is accompanied by the development of acute hyperergic conjunctivitis. At the same time, an abundant outflow of grayish-purulent exudate from the corner of the eye, arterial hyperemia, and swelling of the eyelids are observed.

transplanted tissue rejection as a result of transplantation of foreign tissue, the recipient's lymphocytes become sensitized (become carriers of the transfer factor or cellular antibodies). These immune lymphocytes then migrate to the transplant, where they are destroyed and release the antibody, which causes the destruction of the transplanted tissue. The transplanted tissue or organ is rejected. Transplant rejection is the result of a delayed-type allergic reaction.

Autoallergic reactions - reactions resulting from damage to cells and tissues by autoallergens, i.e. allergens that originate in the body itself.

Bacterial allergy - appears with preventive vaccinations and with certain infectious diseases (with tuberculosis, brucellosis, coccal, viral and fungal infections). If the allergen is administered intradermally to a sensitized animal, or applied to scarified skin, then the response begins no earlier than 6 hours later. At the site of contact with the allergen, hyperemia, induration and sometimes skin necrosis occur. With the injection of small doses of the allergen, necrosis is absent. In clinical practice, delayed Pirquet and Mantoux skin reactions are used to determine the degree of sensitization of the body in a particular infection.

Second classification. Depending on the type of allergen All allergies are divided into:

Serum

infectious

1. Vegetable

   Animal origin

   drug allergy

   Idiosyncrasy

   household allergies

   Autoallergy

Serum allergy. This is such an allergy that occurs after the introduction of any therapeutic serum. An important condition for the development of this allergy is the presence of an allergic constitution. Perhaps this is due to the peculiarity of the autonomic nervous system, the activity of blood histaminase and other indicators that characterize the setting of the body to an allergic reaction.

This type of allergy is especially important in veterinary practice. Anti-erysipelas serum, with inept treatment causes the phenomenon of allergy, anti-tetanus serum can be an allergen, with repeated administration, anti-diphtheria serum can be an allergen.

The mechanism of development of serum sickness is that a foreign protein introduced into the body causes the formation of antibodies such as precipitins. Antibodies are partially fixed on the cells, some of them circulate in the blood. After about a week, the antibody titer reaches a level sufficient to react with a specific allergen for them - a foreign serum that is still preserved in the body. As a result of the combination of the allergen with the antibody, an immune complex arises, which settles on the endothelium of the capillaries of the skin, kidneys and other organs. This causes damage to the endothelium of the capillaries, an increase in permeability. Allergic edema, urticaria, inflammation of the lymph nodes, glomeruli of the kidneys and other disorders characteristic of this disease develop.

infectious allergy – such an allergy, when the allergen is any pathogen. This property may have a tubercle bacillus, pathogens of glanders, brucellosis, helminths.

Infectious allergy is used for diagnostic purposes. This means that microorganisms increase the body's sensitivity to preparations prepared from these microorganisms, extracts, extracts.

food allergy – various clinical manifestations of allergy associated with food intake. The etiological factor is food proteins, polysaccharides, low molecular weight substances acting as haptens (food allergens). The most common food allergies are to milk, eggs, fish, meat and products made from these products (cheeses, butter, creams), strawberries, strawberries, honey, nuts, citrus fruits. Allergenic properties are possessed by additives and impurities contained in food products, preservatives (benzoic and acetylsalicylic acids), food colorings, etc.

There are early and late reactions of food allergies. The early ones develop within one hour from the moment of ingestion, severe anaphylactic shock is possible, up to death, acute gastroenteritis, hemorrhagic diarrhea, vomiting, collapse, bronchospasm, swelling of the tongue and larynx. Late manifestations of allergy are associated with skin lesions, dermatitis, urticaria, angioedema. Symptoms of food allergies are observed in different parts of the gastrointestinal tract. Possible development of allergic stomatitis, gingivitis, damage to the esophagus with symptoms of edema, hyperemia, rashes on the mucous membrane, feeling of difficulty swallowing, burning and pain along the esophagus. The stomach is often affected. Such a lesion is clinically similar to acute gastritis: nausea, vomiting, pain in the epigastric region, tension in the abdominal wall, eosinophilia of gastric contents. With gastroscopy, swelling of the gastric mucosa is noted, hemorrhagic rashes are possible. With intestinal damage, there are cramping or persistent pain, bloating, tension in the abdominal wall, tachycardia, and a drop in blood pressure.

plant allergy – such an allergy, when the allergen is the pollen of a plant. Pollen of bluegrass meadow, cocksfoot, wormwood, timothy grass, meadow fescue, ragweed and other herbs. The pollen of various plants differs from each other in antigenic composition, but there are also common antigens. This causes the development of polyvalent sensitization caused by the pollen of many grasses, as well as the appearance of cross-reactions to various allergens in patients with hay fever.

The allergenic properties of pollen depend on the conditions in which it resides. Fresh pollen, i.e. when it is released into the air from the dust particles of the stamens of grasses and trees, it is very active. Getting into a humid environment, for example, on mucous membranes, the pollen grain swells, its shell bursts, and the internal contents - plasma, which has allergenic properties, is absorbed into the blood and lymph, sensitizing the body. It has been established that grass pollen has more pronounced allergenic properties than tree pollen. In addition to pollen, other parts of plants may have allergenic properties. The most studied of them are fruits (cotton).

Repeated exposure to plant pollen can cause suffocation, bronchial asthma, inflammation of the upper respiratory tract, etc.

Allergy of animal origin- cells of various tissues, components of various structures of a living organism have pronounced allergenic properties. The most significant are epidermal allergens, Hymenoptera poisons and mites. Epidermal allergens consist of integumentary tissues: dandruff, epidermis and hair of various animals and humans, particles of claws, beaks, nails, feathers, animal hooves, scales of fish and snakes. Frequent allergic reactions in the form of anaphylactic shock from insect bites. The presence of cross-allergic reactions caused by insect bites has been shown within the class or species. Insect venom is a product of special glands. It consists of substances with pronounced biological activity: biogenic amines (histamine, dopamine, acetylcholine, norepinephrine), proteins and peptides. Allergens of ticks (bed, barn, dermatophagous, etc.) are often the cause of bronchial asthma. When they enter with the inhaled air, the sensitivity of the body is perverted.

drug allergy - when the allergen is any medicinal substance. Allergic reactions caused by drugs presently present the most serious complications in drug therapy. The most common allergens are antibiotics, especially administered orally (penicillin, streptomycin, etc.). Most drugs are not full antigens, but have the properties of haptens. In the body, they form complexes with blood serum proteins (albumin, globulin) or tissues (procollagen, histone, etc.). This indicates the ability of almost every drug or chemical to cause allergic reactions. In some cases, haptens are not antibiotics or chemotherapy drugs, but the products of their metabolism. Thus, sulfanilamide preparations do not have allergenic properties, but acquire them after oxidation in the body. A characteristic feature of drug allergens is their pronounced ability to cause paraspecific or cross-reactions, which determines the polyvalence of drug allergy. Manifestations of drug allergies range from mild reactions in the form of skin rash and fever, to the development of anaphylactic shock.

Idiosyncrasy - (from Greek . idios - independent, syncrasis - mixing) is an innate hypersensitivity to food or drugs. When taking certain foods (strawberries, milk, chicken protein, etc.) or drugs (iodine, iodoform, bromine, quinine), certain individuals experience disorders. The pathogenesis of idiosyncrasy has not yet been established. Some researchers point out that in idiosyncrasy, unlike anaphylaxis, it is not possible to detect specific antibodies in the blood. It is assumed that food idiosyncrasy is associated with the presence of congenital or acquired increased permeability of the intestinal wall. As a result, protein and other allergens can be absorbed into the blood in an unsplit form and thereby sensitize the body to them. When the body encounters these allergens, an attack of idiosyncrasy occurs. In some people, characteristic allergic phenomena occur mainly from the skin and vascular system: hyperemia of the mucous membranes, edema, urticaria, fever, vomiting.

household allergies - in this case, the allergen can be mold, sometimes fish food - dried daphnia, plankton (lower crustaceans), house dust, household dust, mites. Household dust is the dust of residential premises, the composition of which varies in terms of the content of various fungi, bacteria and particles of organic and inorganic origin. Library dust in large quantities contains remnants of paper, cardboard, etc. According to most modern data, the allergen from house dust is a mucoprotein and a glycoprotein. Household allergens can sensitize the body.

Autoallergy- occurs when allergens are formed from their own tissues. With the normal function of the immune system, the body removes, neutralizes its own, degenerate cells, and if the body's immune system cannot cope, then the degenerate cells and tissues become allergens, i.e. autoallergens. In response to the action of autoallergens, autoantibodies (reagins) are formed. Autoantibodies combine with autoallergens (self-antigens) and form a complex that damages healthy tissue cells. The complex (antigen + antibody) is able to settle on the surface of muscles, other tissues (brain tissue), on the surface of the joints and cause allergic diseases.

According to the mechanism of autoallergy, diseases such as rheumatism, rheumatic heart disease, encephalitis, collagenoses occur (non-cellular parts of the connective tissue are damaged), kidneys are affected.

The third classification of allergies.

Depending on the sensitizing agent There are two types of allergies:

* Specific

* Non-specific

Allergy is called specific if the sensitivity of the organism is perverted only to the allergen with which the organism is sensitized, i.e. there is strict specificity here.

A representative of a specific allergy is anaphylaxis. Anaphylaxis consists of two words (ana - without, phylaxis - protection) and literally translated - defenselessness.

Anaphylaxis- this is an increased and qualitatively perverted response of the body to the allergen to which the body is sensitized.

The first introduction of an allergen into the body is called sensitizing administration, or otherwise sensitizing. The value of the sensitizing dose can be very small, sometimes it is possible to sensitize with such a dose as 0.0001 g of the allergen. The allergen must enter the body parenterally, i.e., bypassing the gastrointestinal tract.

The state of increased sensitivity of the body or the state of sensitization occurs after 8-21 days (this is the time required for the production of class E antibodies), depending on the type of animal or individual characteristics.

A sensitized organism looks no different from an unsensitized organism.

Re-introduction of an antigen is called the introduction of a resolving dose or reinjection.

The size of the resolving dose is 5-10 times higher than the sensitizing dose, and the resolving dose should also be administered parenterally.

The clinical picture that occurs after the introduction of a resolving dose (according to Bezredko) is called anaphylactic shock.

Anaphylactic shock is a severe clinical manifestation of allergy. Anaphylactic shock can develop at lightning speed, within a few minutes after the introduction of the allergen, less often after a few hours. Harbingers of shock can be a feeling of heat, redness of the skin, itching, fear, nausea. The development of shock is characterized by a rapidly growing collapse (pallor, cyanosis, tachycardia, thready pulse, cold sweat, a sharp decrease in blood pressure), suffocation, weakness, loss of consciousness, swelling of the mucous membranes, and convulsions. In severe cases, there is acute heart failure, pulmonary edema, acute kidney failure, allergic lesions of the intestines are possible, up to obstruction.

In severe cases, dystrophic and necrotic changes in the brain and internal organs, interstitial pneumonia, and glomerulonephritis may develop. At the height of shock in the blood, erythremia, leukocytosis, eosinophilia, an increase in ESR are noted; in the urine - proteinuria, hematuria, leukocyturia.

According to the rate of occurrence, anaphylactic shock can be (acute, subacute, chronic). Acute form - changes occur after a few minutes; subacute occurs after a few hours; chronic - changes occur after 2-3 days.

Different animal species do not show the same sensitivity to anaphylactic shock. The most sensitive to anaphylaxis are guinea pigs, and further on the degree of sensitivity, the animals are arranged in the following order - rabbits, sheep, goats, cattle, horses, dogs, pigs, birds, monkeys.

So, guinea pigs have anxiety, itching, scratching, sneezing, the pig rubs its muzzle with its paws, trembles, involuntary defecation is observed, takes a lateral position, breathing becomes difficult, intermittent, respiratory movements slow down, convulsions appear and may be fatal. This clinical picture is combined with a drop in blood pressure, a decrease in body temperature, acidosis, and an increase in the permeability of blood vessels. An autopsy of a guinea pig that died from anaphylactic shock reveals foci of emphysema and atelectasis in the lungs, multiple hemorrhages on the mucous membranes, and unclotting blood.

Rabbits - 1-2 minutes after the introduction of a resolving dose of serum, the animal begins to worry, shakes its head, lies on its stomach, shortness of breath appears. Then there is a relaxation of the sphincters and urine and feces are involuntarily separated, the rabbit falls, bends its head back, convulsions appear, then breathing stops, death occurs.

In sheep, anaphylactic shock is very acute. After the introduction of a permissive dose of serum, shortness of breath, increased salivation, lacrimation occur in a few minutes, pupils dilate. Swelling of the scar is observed, blood pressure decreases, involuntary separation of urine and feces appear. Then there are paresis, paralysis, convulsions, and often the death of the animal occurs.

In goats, cattle, and horses, the symptoms of anaphylactic shock are somewhat similar to those in the rabbit. However, they most clearly show signs of paresis, paralysis, and there is also a decrease in blood pressure.

Dogs. Essential in the dynamics of anaphylactic shock are disorders of the portal circulation and blood stasis in the liver and intestinal vessels. Therefore, anaphylactic shock in dogs proceeds according to the type of acute vascular insufficiency, at first there is excitement, shortness of breath, vomiting occurs, blood pressure drops sharply, involuntary separation of urine and feces, mostly red (an admixture of erythrocytes), appears. Then the animal falls into a stuporous state, while there is a bloody discharge from the rectum. Anaphylactic shock in dogs is rarely fatal.

In cats and fur-bearing animals (Arctic foxes, foxes, minks) similar dynamics of shock is observed. However, arctic foxes are more susceptible to anaphylaxis than dogs.

Monkey. Anaphylactic shock in monkeys is not always reproducible. In shock, monkeys experience difficulty in breathing, collapse. The number of platelets falls, blood clotting decreases.

In the occurrence of anaphylactic shock, the functional state of the nervous system matters. It is not possible to cause a picture of anaphylactic shock in anesthetized animals (narcotic blocking of the central nervous system turns off impulses going to the site of allergen introduction), during hibernation, in newborns, with sudden cooling, as well as in fish, amphibians and reptiles.

Antianaphylaxis- this is a state of the body that is observed after suffering anaphylactic shock (if the animal has not died). This condition is characterized by the fact that the body becomes insensitive to this antigen (allergen within 8-40 days). The state of anti-anaphylaxis occurs 10 or 20 minutes after anaphylactic shock.

The development of anaphylactic shock can be prevented by administering small doses of the antigen to the sensitized animal 1-2 hours before the injection of the required volume of the drug. Small amounts of antigen bind antibodies, and the resolving dose is not accompanied by the development of immunological and other stages of immediate hypersensitivity.

Nonspecific Allergy- this is such a phenomenon when the body is sensitized to one allergen, and the sensitivity reaction to another allergen is perverted.

There are two types of nonspecific allergies (paraallergy and heteroallergy).

Paraallergy - they call such an allergy when the body is sensitized by one antigen, and sensitivity increases to another antigen, i.e. one allergen increases the sensitivity of the body to another allergen.

Heteroallergy is such a phenomenon when the body is sensitized by a factor of non-antigenic origin, and the sensitivity increases, perverts to any factor of antigenic origin, or vice versa. Factors of non-antigenic origin can be cold, exhaustion, overheating.

Cold can increase the body's sensitivity to foreign proteins, antigens. That is why in a state of cold, serum should not be administered; the flu virus shows its effect very quickly if the body is supercooled.

Fourth classification -according to the nature of the manifestation allergies are distinguished:

General- this is such an allergy, when, with the introduction of a resolving dose, the general condition of the body is disturbed, the functions of various organs and systems are disrupted. To obtain a general allergy, a single one-time sensitization is sufficient.

local allergy - this is such an allergy when, with the introduction of a resolving dose, changes occur at the injection site of the allergen, and at this site can develop:

hyperergic inflammation

ulceration

skin fold thickening

swelling

To obtain a local allergy, multiple sensitization is required with an interval of 4-6 days. If the same antigen is injected several times into the same place of the body with an interval of 4-6 days, then after the first injections, the antigen dissolves completely, and after the sixth, seventh injection, swelling, redness occurs at the injection site, and sometimes inflammatory reaction with extensive edema, extensive hemorrhage, i.e. local morphological changes are observed.