Immunology is the science of immunity. She studies the manifestation, mechanisms and methods of managing immunity, and also develops immunological methods for the diagnosis, treatment and prevention of diseases in humans and animals.

It is believed that the beginning of a new science was laid by the famous experiments of the English physician E. Jenner (1749-1823). He noticed that during epidemics of human smallpox, milkmaids most often do not fall ill. As you know, cows suffer from smallpox with skin lesions, especially the skin of the udder and nipples, where smallpox pustules develop. Milkmaids who contract cows with smallpox develop pustules on their hands. Observing these phenomena, Jenner came to the conclusion that after infection and illness of milkmaids with cowpox, they become immune to infection with human smallpox. In confirmation of his observations, in May 1796, he inoculated an 8-year-old boy first with cowpox, and after 1.5 months, human smallpox, and the boy did not fall ill. However, Jenner did not see the principle of protection against other infectious diseases in the method of combating smallpox that he discovered. His discovery gave humanity only a way to prevent smallpox.

Louis Pasteur is recognized as the founder of modern scientific immunology. In 1881, he reported that chickens, when infected with a weakened pathogen of chicken cholera, become immune to infection with virulent cultures. Comparing his experiments with Jenner's observations, Pasteur formulated the basic principle of protection against the causative agent of any infectious disease, which is that the body, after meeting with a weakened pathogen, becomes immune (immune) to virulent microbes of the same species. In honor of Jenner, the discoverer of smallpox vaccinations, Pasteur named the weakened cultures of pathogens vaccines (from the Latin vacca - cow). In subsequent years, Pasteur made vaccines and, when immunizing animals, established the presence of immunity against diseases such as anthrax, rabies, erysipelas, etc. Later it was found that immunity can be created by vaccination with killed microorganisms, as well as toxins secreted by microorganisms.

By the end of the 19th and the beginning of the 20th centuries, many discoveries were made that created the scientific foundation of immunology. In 1883 I. Mechnikov discovered phagocytosis and introduced the concept of "cellular immunity". During these years, the humoral theory of immunity was also developed, of which P. Ehrlich was a supporter. Long-term controversy between supporters of the cellular and humoral theories of immunity contributed to the formation of immunology as a science. In 1908, Mechnikov and Ehrlich were awarded the Nobel Prize for outstanding discoveries in immunity. In 1891 E. Bering and S. Kitazato first applied passive immunization against diphtheria and tetanus; in 1900 K. Landsteiner discovered blood groups (A, B, O) in humans; in 1902 C. Richet established the phenomenon of anaphylaxis; in 1905 K. Pirke introduced the concept of "allergy"; in 1953 P. Medovar and M. Hasek independently discovered the phenomenon of immunological tolerance; in 1958 F. Burnet proposed a clonal selection theory of immunity; in 1959 J. Doss et al. discovered the system of antigens of the histoses of human revenge; in 1962 F, Miller established the role of the thymus as a primary lymphoid organ; in 1963 B. Benacerraf established genes of immunoreactivity, called Ir-genes; in N975, C. Milstein and D. Kehler proposed a method for obtaining monoclonal antibodies. The largest generalization of recent years was the isolation of two independent, but jointly functioning cell populations in the immune response of T and B lymphocytes.

As a result of new discoveries and achievements, immunology has grown into an independent scientific discipline covering the range of problems of modern biology, medicine and veterinary medicine. The areas of general immunology include molecular immunology, immunomorphology, immunogenetics, immunochemistry, evolutionary immunology, and among the areas of private immunology - immunoprophylaxis of infectious diseases, clinical immunology, immunology of reproduction and embryogenesis, immunopathology, immuno-oncology, transplant immunology.

Veterinary immunology is also developing in all leading areas of immunology in general. Special attention in immunology is paid to the study of the characteristics of immunity in farm animals and the search for effective means and methods of their immune protection. In recent years, more than 180 different biological products (vaccines, serums, diagnosticums) have been prepared for veterinary practice.

The formation and further development of veterinary immunology in our country was facilitated by the works of the most prominent scientists N.N. Ginsburg, S.N. Vyshelesky, A.A. Vladimirov, S.G. I. Kulesko, N. V. Likhachev, S. Ya. Lyubashenko, N. A. Mikhina, S. A. Muromtseva, A. Kh. Sarkisov, P. S. Solomkin and many others. Veterinary immunology is faced with major tasks to create new and improve existing vaccines, serums and yes gnostic minds, to study and prevent immune diseases, to expand research in the field of non-infectious immunology (age-related immunology, immunology of reproduction, nonspecific mechanisms of resistance).

VETERINARY MICROBIOLOGYAND IMMUNOLOGY

for the specialty 310800 - "Veterinary medicine" according to the qualifications of a specialist - a veterinarian

Moscow 2001

1. Goals and objectives of the discipline "veterinary microbiology and immunology"

The main goal of teaching the discipline "Veterinary Microbiology and Immunology" is the formation of a future veterinarian's scientific worldview about the diversity of microorganisms, about their role in general biological processes, incl. in case of infections, and in animal pathology, the development of the theoretical foundations of the diagnosis of infectious diseases, the principles of immunological research, the manufacture and control of biological products.

The objectives of the course include the study by students of the principles: taxonomy, morphology and physiology, latitude_ of distribution of microorganisms in nature, the characteristics of their biology and ecology; the role of microbes in the transformation of substances in nature and the effects of environmental factors on prokaryotic cells, mastering the basics of the doctrine of infection and immunity, heredity and variability, mastering the methods of indication and identification of bacteria and fungi pathogenic for animals, bacteriological serological, genetic and allergic studies used in the diagnosis of infectious diseases.

As a result of studying the course, students should know the theoretical foundations of the vital activity of microorganisms, their interaction with each other and with the body of animals, the basic biological properties of pathogenic microbes, the principles and methods of diagnosis and specific prevention of infectious diseases. The educational and research work of SUIRS students contributes to these goals and objectives.

The knowledge gained on the biology and ecology of pathogens of infectious diseases, infections and immunity should help future veterinary specialists to properly organize and conduct bacteriological and serological studies, specific prophylaxis of infectious diseases. To study the course "Veterinary Microbiology and Immunology", students need to master the sections of the following disciplines:

physics (jet propulsion in living organisms, centrifuges and their application in biological research, cell mem-

branes, resolution of optical devices, luminescence analysis, photobiological reactions, X-ray radiation, electron microscope);

organic chemistry (hydrocarbons, alcohols, phenols, carbohydrates, amino acids and proteins);

inorganic and analytical chemistry (dispersed systems and solutions, preparation of dilutions with coefficients 2 and 10);

physical and colloidal chemistry (the doctrine of solutions, the mechanism of photosynthesis, the stability of colloidal systems and coagulation, suspensions, emulsions and foams, proteins);

anatomy of farm animals (organs of blood and lymph formation);

biochemistry (enzymes, proteins, biological oxidation and bioenergy elements, structure and properties of carbohydrates, classification, structure and basic properties of lipids, structure and synthesis of amino acids and nucleoproteins, biological value of vitamins, water metabolism and metabolism of mineral substances);

Physiology, pathophysiology (transport of nutrients, mechanisms of secretion, general biological terms, mechanism of inflammation, allergies, actions of lysozyme, complement, organs and cells of the immune system).

Naturally, knowledge of the Latin language is necessary for a more successful mastering of courses in microbiology and immunology.

The instructors check the mastery of the discipline by students in laboratory classes, colloquia (orally or using a computer program), on written tests and coursework, offsets, and at the end of courses - exams.

Textbook. - M .: Agrovet, 2011 .-- 752 p .: ill. - ISBN 978-5-905543-01 -2. The book describes in detail the main stages of the formation and development of immunology, incl. in Russia, information about the Nobel laureates in immunology is presented. Modern ideas about the structural and functional structure of the immunity of animals, birds and humans are given. The processes of differentiation and functioning of the central cells of the immune system - T- and B-lymphocytes at the organismal, cellular and molecular levels are characterized; functionally different subpopulations of these cells with effector, helper and suppressor activity are described. Modern concepts of antigens and isoantigens (leukocytes, erythrocytes), products of resting and activated cells of the immune system and immunologically significant membrane molecules of these cells (cytokines, immunoglobulins, receptor apparatus, molecules of adhesion, coreception, costimulation, etc.) are given. Various forms and mechanisms of formation of reactions of humoral and cellular immunity, including transplantation, mechanisms of formation of tolerance (central, peripheral, oral), elimination of "forbidden" clones, etc. are shown. The important role of the genetic apparatus of individuals, which controls the maintenance of immunological homeostasis, is shown. Much attention is paid to the histocompatibility complex and its biological functions. The features of innate immunity and the mechanisms of its functioning are described in detail - effector cells (macrophages, natural killer cells), the mechanisms of recognition by the pattern-recognizing PRR receptors of the PAMP structures of microbes (molecular mosaic of the pathogen), the importance of physical, chemical and humoral factors in the reactions of innate immunity. The role of innate immunity reactions in the formation of adaptive immunity is shown. ILL lymphocytes (Innate-like lymphocytes), which play an important role in innate immune responses and function as primary barriers of the immune system - B1-, MzB-, MAIT-, γδТ- and NK-T-lymphocytes, have been characterized.
The textbook is intended for students, graduate students, residents, teachers of veterinary and biological faculties of universities, courses and departments for advanced training of veterinarians and biologists, for scientists, specialists in various fields interested in the problems of immunology. Organs and lymphoid tissue of the immune system of CX animals and birds.
Cells of the immune system: hematopoietic stem cells.
T-lymphocytes.
B-lymphocytes.
Natural killer cells (NK lymphocytes) and T lymphocytes with natural killer cell activity (NKT lymphocytes).
Dendritic cells. Cells of the mononuclear phagocyte system. Granulocytes.
Antigens.
Congenital immunity.
Adaptive immunity. Reactions of the humoral type.
Intracellular signaling pathways and activation of animal and human cells.
Antibodies and their formation in animals and birds.
Major histocompatibility complex and biological significance. Genetic diversity and features of the formation of the antigen-recognizing repertoire of t- and b-lymphocytes.
Cytokines.
Cellular immunity.
Immunological tolerance.
Immunological deficiency.
Immunomodulators are medicines for the immune system.
Model systems in immunology.
Immunobiotechnology.

FEDERAL STATE BUDGET EDUCATIONAL DEPARTMENT OF HIGHER PROFESSIONAL EDUCATION

MOSCOW STATE ACADEMY OF VETERINARY MEDICINE AND BIOTECHNOLOGY them. K. I. SKRYABINA

____________________________________________________________

V. N. Denisenko

VETERINARY

IMMUNOPATHOLOGY

LECTURE

MOSCOW, 2011

UDC 619: 616-097.3 (07)

Kruglova immunopathology. Lecture. - Moscow .: FGBOU VPO MGAVMiB im. , 2011, 30 p.

The paper presents materials reflecting the protective reactions of the body's immune system, as well as immunodeficiency states. Role shown allergic and autoimmune reactions, as well as immune complexes in the development of the pathological process in non-infectious diseases of animals.

The lecture is intended for students of full-time, part-time and part-time (evening) faculties veterinary medicine, students of the faculty of advanced training and practicing veterinarians.

Reviewer: Petrov A. M., doctor wind. Sciences, Professor of the Moscow State Academy of Medical Sciences ...

Gavrilov V. A., doctor wind. Sciences, Professor of the Moscow State Academy of Medical Sciences

The lecture was approved at a meeting of the educational and methodological commission of the Faculty of Veterinary Medicine (Protocol No.

1. Introduction

2. Defense reactions of the body's immune system

3. Immunodeficiency states

4. Allergy

5. Diseases of animals, the pathogenesis of which is caused by allergic reactions

6. Immunological tolerance

INTRODUCTION

The immune system maintains the body's homeostasis. It recognizes genetically foreign substances, neutralizes and eliminates them, and prevents re-entry into the body. However, in some cases, substances produced by immune responses can damage the cells and tissues of the host and thus cause disease in animals.

Of the immune pathologies among animals, weakening of immune reactivity (immunodeficiencies) and allergies (atopy) are more common than others. Allergies refer to atypical immune responses that are characterized by an increase, complication and acceleration of the immune response.

In recent years, the role of immune responses in animal pathology has increased markedly. Immunodeficiency states play a leading role in the wide spread of animal diseases caused by opportunistic microorganisms

Allergic reactions are involved in the pathogenesis of anaphylactic shock, serum sickness, acute glomerulonephritis, allergic rhinitis, bronchitis, dermatitis. They complicate the course of many infectious and invasive diseases.

The development of allergies is associated with damage to lymphoid tissue, violation of mechanisms immunological the reactivity of the body, a change antigenic properties of host tissues, the presence of an excessive amount of immune complexes.

An essential role in animal allergization is attributed to environmental pollution, the emergence of new synthetic substances, food preservatives and additives.

Immune defense mechanisms

The immune system is represented by a set of organs, tissues and cells that react to the ingress of genetically foreign substances into the body - antigens. Antigenic properties are possessed by microorganisms and their metabolic products, foreign proteins, polysaccharides, nucleoproteins, insect toxins, and plant pollen.

The morphological basis of the immune system is lymphoid tissue. It forms the parenchyma of the spleen, thymus and lymph nodes. Clusters of lymphocytes are found under the mucous membrane of the intestines, pharynx, bronchi, genitourinary system, salivary and lacrimal glands and other tissues. In the blood of various animal species, lymphocytes make up from 21 to 65% of all leukocytes.

Some of the lymphocytes circulate from the blood to the tissues and vice versa. Lymphocytes were not found in the brain tissue of healthy animals.

In addition to lymphocytes, mononuclear phagocytes in the form of tissue macrophages and blood monocytes, as well as eosinophils, neutrophils and mast cells, take part in the implementation of immune reactions.

The cells of the immune system synthesize substances - interleukins, lymphokines, etc., which play the role of mediators in immune reactions.

Immune reactions develop after the introduction of an antigen into the body. An active physiological immune response includes the recognition of an invaded antigen as a foreign substance, disintegration its macrophages and transmission of antigenic information to immunocompetent cells. As a result of the reaction of the latter, humoral and cellular mechanisms of immunity are formed.

Humoral mechanism immune response is associated with the formation antibodies... Antibodies are synthesized by plasma cells, which are formed from B-lymphocytes. In the first phase of the immune response, high-molecular-weight IgM are synthesized, then IgG and IgA. Class A immunoglobulins penetrate the surface of the mucous membranes, combine with secretory proteins and become resistant to the action of the proteolytic enzymes pepsin and trypsin.

The protection of the mucous membranes is provided mainly by secretory IgA. In recent years, it has been proven that a significant part of secretory antibodies are IgG. Antibodies play a leading role in the antibacterial and antitoxic defense of the body.

Immunoglobulins of class E are found in blood serum of healthy animals in small amounts. They play an important role in the formation of immunopathological reactions, in particular allergies. In animals with allergies, their serum content is higher than in healthy animals.

Natural resistance... Inborn nonspecific factors of natural resistance play an important role in the defense of the organism. They provide general protection for the body. The action of natural resistance factors is aimed at neutralizing all or several antigens. Non-specific protection is provided by cellular and humoral factors.

Cellular factors of natural resistance include phagocytic cells - neutrophils and monocytes. The humoral factors of natural resistance are the complement and properdin systems, lysozyme, interferons, lactoferrins, and other substances.

The factors of natural resistance and immunity interact with each other in the body's defense reactions.

Diseases of the immune system

Lymphoid tissue can be affected by physical, chemical and biological factors. Diseases of the immune system are manifested in the form of a decrease in the body's immunological reactivity (immunodeficiencies), atypical immune reactions (allergies) or lack of immune responses (tolerance).

Immunodeficiencies

Immunodeficiency states are characterized by a decrease in the body's immune reactivity. They are classified as primary and secondary. Colostral and age-related immunodeficiencies are considered separately.

Distinguish between deficiency of cellular (T-dependent), humoral (B-dependent) immunity and combined immunodeficiency.

Deficiency of humoral immunity- hypo - and agammaglobulinemia is characterized by a decrease in the synthesis or an increase in the destruction of immunoglobulins. In this case, the concentration of B-lymphocytes can be reduced to a complete absence, the content of IgG and IgA is at a low level. In other cases, the content of B-lymphocytes remains normal, but they synthesize only IgM.

Deficiency of immunoglobulins is established in cattle, pigs, sheep, fur animals, dogs: IgA deficiency has been described in beagles and sharpei, and IgM in Dobermans.

Deficiency of cell-mediated immunity characterized by a low content of T-lymphocytes. More often it is a consequence of a lesion of the thymus and a violation differentiation lymphoid tissue.

Pathogenesis ... Primary immunodeficiencies are associated with a genetically determined deficiency in the development of immunocompetent cells. In animals, due to breeding work, this form of immunodeficiency is rare.

Secondary immunodeficiency states develop as a result of damage to immunocompetent cells by biological, chemical and physical factors. They are noted after animals have recovered from infectious and invasive diseases, after the use of certain drugs, with radioactive irradiation, with a deficiency in the diet of protein, vitamins, trace elements, after surgical operations, over-exploitation, as a result of stress.

Colostral immunodeficiency states are noted in newborn animals. Their development is associated with a violation of the technology of drinking colostrum, its insufficient amount, a decrease in the concentration of immune factors in colostrum and a violation of the ability to assimilate colostrum in offspring. The time of the first drinking of colostrum is of particular importance. Thus, newborn calves absorb the bulk of colostral immunoglobulins in the first 3-4 hours of life.

By the third day of life, they completely lose the ability to assimilate colostrum immunoglobulins. The ability of calves to assimilate colostrum lymphocytes in the first hours of life has also been proven. The transfer of cells contained in colostrum from the intestine to the blood of the calf occurs due to a change in the structure of the walls of the digestive tube, the appearance of "hatches" in it.

Combined immunodeficiency is characterized by impaired cellular and humoral immunity. X-linked combined immunodeficiency in bassetts has been described in the literature.

In young cattle, an age-related deficiency of humoral and cellular immunity factors has been established. In calves at the age of 14-20 days, it is associated with the depletion of colostral and insufficient synthesis of their own immunoglobulins. A decrease in immunological reactivity at 5-6 months of age is associated with a change in the diet and conditions of animals.

Immunodeficiency in older animals is explained atrophy thymus.

Clinical picture immune deficiency is manifested by an increase in the incidence of diseases in animals. Diseases are caused by both pathogenic and opportunistic pathogens. They have a chronic recurrent course, are difficult to treat and often end in death or forced slaughter. In young animals, the respiratory and digestive systems are usually affected, in cows - the genitals. Surgical and accidental wounds suppurate, heal poorly, and pustular lesions of the skin and mucous membranes are also noted.

In bitches and cats, mucopurulent discharge from the vagina is observed, in males - from the prepuce.

Laboratory research ... The presence of an immunodeficiency state is confirmed by laboratory studies of indicators characterizing the body's immune reactivity.

A general clinical blood test reveals an absolute and relative decrease in the concentration of lymphocytes in immunodeficient animals.

More objectively reflect the state of immune reactivity data on the percentage of undifferentiated (zero), B - and T-lymphocytes. In cows, it is 42, 24 and 34%, respectively. A decrease in the specific gravity of immunocompetent cells (T - and B-lymphocytes) indicates the presence of immunodeficiency.

In immunodeficient animals, a decrease in the concentration of immunoglobulins of classes G, M and A, complement, lysozyme, properdin is also noted. After immunization in such animals, the titers of antibodies to vaccine antigen.

A stable indicator of cellular immunity deficiency is a decrease in the swallowing and, especially, the digesting activity of neutrophils and monocytes.

Treatment and prevention ... Treatment of immune deficiency is aimed at eliminating etiological factors and normalizing the mechanisms of immune reactivity.

The fight against immune deficiency includes selection work, providing animals with a full diet, compliance with zoohygienic requirements for maintenance, and regular exercise. Timely preventive measures are taken against infectious diseases.

Of medications with therapeutic and prophylactic purposes, immunomodulators are used, which normalize the processes of proliferation and differentiation of lymphoid tissue. These include T-activin, B-activin, fosprenyl, thymogen, etc.

The use of vitamin preparations, protein hydrolysates, microelements normalizes the body's immunological reactivity. It is recommended to use levamisole to stimulate cellular immunity.

For the prevention of colostral immunodeficiency, it is necessary to properly feed colostrum to newborn animals, especially in the first days of life.

Allergy

The term "allergy" (from the Greek allos - other, ergon - action) was first introduced by Pirquet in 1904. Allergy is characterized by an increase and perversion of the body's immune responses with repeated injections of the antigen. Antigens causing allergic reactions are called allergens.

There are exo - and endoallergens. Exoallergens - foreign proteins, complex compounds, waste products of microorganisms, protozoa, insect toxins, drugs, plant pollen, artificially synthesized substances. They enter the body from the external environment.

Endoallergens (autoallergens) are contained and formed in the body. Allergy is caused by tissues of the barrier organs (brain, testes, vitreous humor, thyroid gland) when the barriers are damaged. The properties of allergens are acquired by host proteins, denatured under the influence of physical, chemical and biological factors. Tissues of the heart in rheumatic myocarditis, kidneys - in chronic nephritis, liver - in chronic hepatitis, bronchi - in chronic bronchitis, skin - in case of burns and frostbite cause allergic reactions.

Classification of allergic reactions

The first classification of allergies was proposed by R. Cook in 1930. In 1969 P. Jell and R. Coombs developed a classification that takes into account the nature of all immunopathologies.

R. Cook's classification takes into account the time of the appearance of the body's reaction after repeated administration of the allergen. According to this classification, all allergic reactions are divided into two groups: immediate hypersensitivity (HST) and delayed hypersensitivity (HRT) types.

GNT reactions develop no later than 2 hours, and more often a few minutes after re-administration of the allergen.

HRT develops within 24 hours and later after repeated contact with the antigen. Delayed-type hypersensitivity reactions include infectious allergy in tuberculosis, brucellosis.

The classification of P. Gell and R. Coombs covers all known forms of immunopathology. According to this classification, all allergic reactions are divided into four types.

I a type (anaphylactic) refers to GNT. It is characterized by the fact that during initial contact with the allergen, the body produces a large amount of specific immunoglobulins of class E. Normally, JgE is contained in an insignificant amount. These immunoglobulins with their Fc fragments are fixed on receptors located on the membranes of mast cells and basophils. When the allergen re-enters the body, it is bound by two IgE molecules fixed on the membranes of mast cells. The result is activation mast cells, accompanied by the release of biologically active substances from it - histamine, serotonin, bradykinin. These substances are inflammatory mediators.

Type I allergic reaction forms the basis of the pathogenesis of such diseases as anaphylactic shock, allergic dermatitis (urticaria), allergic rhinitis, conjunctivitis, bronchitis and atopic bronchial asthma, drug intolerance, Quincke's edema.

II a type - cytotoxic. It is characterized by immune lysis of the body's own cells in which the antigenic structure of cell membranes is altered. A change in the antigenic properties of cells occurs when viruses, bacteria, and their metabolic products adhere to them. The antigenic properties of cell membranes can change some medicinal substances - heparin, sulfonamides, barbiturates, acetylsalicylic acid, antibiotics penicillin series. Such cells stimulate the production of antibodies of the IgG and IgM classes. These antibodies form immune complexes with cell antigens, which activate the complement system. As a result of activation, the last components of the complement system (C8- and C9-) acquire the properties of enzymes. The latter lyse cells with altered antigenic structure. Currently, the body's autoimmune reactions are associated with type II allergic reactions. Allergic reaction of type II underlies the pathogenesis of autoimmune hemolytic anemia, leukopenia, thrombocytopenia, autoimmune atrophic gastritis, autoimmune pancreatitis, chronic active hepatitis.

III a type due to the excessive formation of immune complexes: antigen-antibody and activation of the complement system. The formation of immune complexes is a physiological form of binding and removing antigens from the body. Normally, immune complexes are metabolized by phagocytosis and excreted in the urine. In case of violation of the catabolism of immune complexes, which is noted with their excess amount, type III allergy develops.

Immune complexes are formed when exo - and endoantigens bind to precipitating IgG and IgM antibodies. Antigens can be hyperimmune sera, gammaglobulins, bacterial and viral metabolic products, some drugs, as well as modified host cells.

Difficultly soluble complexes formed with an excessive amount of polyvalent antigens - lipopolysaccharides and proteins - have the greatest damaging effect.

The damaging effect of these complexes is associated with biologically active substances that are formed during the activation of complement (C3 and C5 convertases). In addition, immune complexes activate cells carrying Fc and C receptors. In this case, neutrophils and macrophages secrete lysosomal enzymes, mast cells - histamine.

Immune complexes are more often deposited on blood vessels, where there is increased pressure or areas of turbulent blood flow - capillaries of the renal glomeruli, choroid, skin, serous and synovial membranes. In this regard, they cause such immunocomplex diseases as glomerulonephritis, serum sickness, uveitis, allergic vasculitis, rheumatoid arthritis.

With the local formation of immune complexes, the Arthus reaction develops. It is observed in actively or passively immunized animals after subcutaneous administration of antigen or antibodies, and is characterized by vascular-necrotic processes. After 4-10 hours, vasculitis develops at the injection site, then after the destruction of the basement membrane of the capillaries by lytic factors, the blood cells and the above-described biologically active substances pass into the extravascular space. They cause vascular reactions, necrosis and tissue lysis. The Arthus reaction is often noted with hyperimmunization of animals.

IV type (cellular) refers to delayed-type hypersensitivity (HRT). It is characterized by a local inflammatory reaction at the site of contact of sensitized lymphocytes with the antigen.

With intradermal administration of antigen, the first signs of HRT are erythema, edema that appears after 6-8 hours and after 24-48 hours they reach a peak.

The HRT reaction begins with the arrival of monocytes at the site of contact with the antigen. They phagocytose antigen and provide information about it to T cells. T cells recognize the antigen and secrete a soluble factor that stimulates the release of histamine and serotonin from mast cells. These mediators increase the permeability of blood capillaries, which contributes to the entry of monocytes and macrophages into the focus, which phagocytose the antigen. In the chronic course of HRT, a granuloma is formed, which consists of macrophages, lymphocytes, plasma cells, neutrophils and eosinophils.

Diseases of animals, the pathogenesis of which is caused by allergic reactions

Immediate hypersensitivity (HNT) can clinically manifest itself in the form of systemic or local lesions of the organs of the animal. Systemic pathologies include anaphylactic shock (anaphylaxis), local ones - hay fever, allergic dermatitis, rhinitis, conjunctivitis, bronchitis, bronchial asthma, food intolerance.

Anaphylactic shock

Anaphylactic shock in animals develops as a result of an allergic reaction of type I (HNT). The disease proceeds quickly with involving the main systems of the body and in the absence of medical care can be fatal. Anaphylactic shock occurs in all animal species.

Etiology... In animals, anaphylactic shock can develop after re-immunization against bacterial and viral diseases, with repeated use of antibiotics, sulfanilamides and other drugs, with the use of hyperimmune sera and immunoglobulins from donated blood. There is an anaphylactic reaction to feed. Poisons of bees, wasps, hornets, and fungal spores can act as allergens.

Pathogenesis. After the initial ingress of the allergen into the animal's body, antibodies are synthesized, which belong to the IgE class. IgE antibodies with their Fc fragments are fixed on the corresponding receptors of mast cells and basophils. The specified stage of an allergic reaction proceeds without the manifestation of clinical signs and pathochemical changes.

When the antigen is reintroduced into the body of a sensitized animal, it binds to antibodies of the IgE class. In this case, an antigen-antibody complex fixed on mast cells and basophils is formed.

These immune complexes stimulate the release of a mediator by mast cells and basophils - histamine, serotonin, eosinophilic and neutrophilic chemotactic factors. Simultaneously with this, the synthesis of new mediators is started - the factor of activation of platelets, prostaglandins, lysosomal enzymes, leukotrienes.

Histamine causes contraction of smooth muscles, increased vascular permeability and blistering, increased secretion of mucus by goblet cells, expansion of arterioles and capillaries.

Serotonin causes spasm of blood vessels of the heart, brain, lungs, kidneys, contraction of smooth muscles.

ProstaglandinsF2 a stimulate the release of mediators by mast cells.

Platelet activating factor activates platelet aggregation and release of serotonin by them, stimulates bronchial spasm, increases vascular permeability and blistering.

Clinical picture . Clinical signs of anaphylactic shock appear immediately after repeated contact with the allergen or after a few minutes. The time of their manifestation depends on the quality of the allergen and on the method of its introduction into the animal's body. In particular, with intravenous administration, signs of GNT appear during the procedure. Anaphylactic shock occurs systemically, that is, with the involvement of the respiratory system, cardiovascular system, liver, skin and mucous membranes, intestinal damage.

The main clinical signs are in the form of rhinitis, conjunctivitis, asthma, pruritus. Tonic and clonic convulsions, spasms of smooth muscles of the bronchi, bronchioles, intestines, edema of the mucous membranes and increased secretion of intestinal glands and bronchi are noted. Expansion and increased permeability of blood vessels leads to pulmonary edema, liver overflow with blood. There is shortness of breath, involuntary discharge of feces and urine, bradycardia, profuse discharge of mucus from the nasal passages.

In cattle, continuous ruminant movements, the release of a frothy liquid from the oral cavity, and acute tympanic scarring are observed. Horses are characterized by anemia mucous membranes, dilated nostrils, wheezing difficulty, heart failure, pulmonary edema.

The disease proceeds super-acutely and in the absence of immediate veterinary care ends with the death of the animal from suffocation, heart and lung failure.

Pollinosis (hay fever)

Pollinosis is an allergic disease that occurs according to the first type of allergy. The clinical manifestation of hay fever is characterized by seasonal allergic rhinitis, allergic conjunctivitis, allergic sinus inflammation, allergic bronchitis and allergic dermatitis.

Clinical manifestations of hay fever largely depend on the method of introducing the allergen into the animal's body. In particular, with parenteral administration of a large amount of the same allergens that, upon inhalation, cause a local reaction, anaphylactic shock may occur.

Etiology . The main etiological factor of hay fever is pollen from wind-pollinated plants. About 60 species of plants are known in the world, the pollen of which causes hay fever. The pollen of these plants is extremely small, so it is easily carried by the wind over long distances. The penetration of pollen into the body of animals and humans occurs with the help of an enzyme contained in it. The disease is seasonal; the first period of rise - spring, associated with flowering trees, the second - summer, associated with flowering of meadow grasses, the third - autumn, associated with flowering of weeds.

In addition to plant pollen, allergens are mold spores that affect straw, hay, and grain waste. The clinical picture of hay fever can be caused by some drugs, the excrement of house mites, the epidermis of the skin and animal hair contained in house dust.

Allergic inflammation in some cases simultaneously affects the skin and mucous membranes of the eyes and respiratory tract, in others - separate systems.

Allergic dermatitis

Allergic dermatitis, the pathogenesis of which is due to type I allergic reaction, is characterized by hyperacute inflammation of the skin and subcutaneous tissue.

The disease occurs in the form of urticaria or inflammatory vascular edema. It can occur in combination with allergic rhinitis and bronchitis.

Etiology ... The disease develops quickly, within a few minutes, after repeated contact of the animal with the allergen. The allergen can enter the body by the oral or parenteral route. An allergic reaction can develop after skin contact with an allergen. Allergens are epidermal cells, tick feces, some types of food, fungal spores, pollen, bee and insect venoms, toxins and metabolic products of microorganisms, antibiotics, hormones, vitamins, food colors, preservatives and antioxidants. In dogs, horses and cattle, allergic dermatitis occurs after the use of protein preparations, vaccines, after blood transfusions, and in some infectious diseases. In pigs, they appear as a result of intensive feeding with fishmeal. Contact allergic dermatitis can be caused by harnesses, collars, care items, ointments, and sprays.

Pathogenesis . The disease is associated with mast cell degranulation caused by the IgE-antigen immune complex and the release of a large number of inflammatory mediators into the blood.

Clinical picture . With the manifestation of allergic dermatitis in the form of urticaria, rashes can appear on different parts of the body. The rash is accompanied by severe itching of the skin. Urticaria is characterized by the formation of blisters on the skin with uneven raised borders, surrounded by a zone of edema and hyperemia. Blisters can merge with each other.

At histological the study of the affected skin areas note loosening collagen fibers, dilation of blood vessels and the presence of perivascular infiltrates, consisting of lymphocytes, eosinophils and neutrophils. After eliminating the action of the allergen, the rashes disappear within 24 hours.

With the clinical manifestation of allergic dermatitis in the form of inflammatory vascular edema, there is hyperemia and edema of certain areas of soft tissues, edema can spread to the mucous membranes. Inflammatory vascular edema, which captures large areas and spreads not only to the dermis, but also to the subcutaneous tissue, is called Quincke's edema. Local dermatitis can occur upon contact with an allergen. When contact with the allergen is eliminated, the signs of allergic dermatitis disappear within 12-24 hours. In case of allergic dermatitis, eosinophilia and leukopenia are noted in the study of blood.

Allergic rhinitis

Allergic rhinitis is an inflammation of the nasal mucous membranes that occurs after inhalation of an allergen. The disease can be seasonal or occur regardless of the season of the year.

Etiology . The development of seasonal rhinitis is due to contact with plant pollen. The cause of perennial rhinitis is the allergens with which the animal is constantly in contact. These include mold spores, epidermis of other animal species, house dust, and industrial waste. Allergic rhinitis often affects animals suffering from other forms of allergy.

It is believed that allergens with a size of 10-100 microns settle on the nasal mucosa and cause allergic rhinitis, smaller allergens reach the bronchi and can cause allergic bronchitis and asthma.

Pathogenesis ... Under the action of enzymes of the nasal mucosa, especially lysozyme, the outer shell of pollen, spores and other allergens is destroyed, which leads to the release of proteins, the molecular weight of which is. Allergens bind to mast cells located in large numbers around the entire submucosal layer, which are sensitized by homologous antibodies of the IgE class. Antibodies of the IgE class specific to allergens are contained not only on mast cells, but also on basophils. Histamine and other mediators of inflammation, which are secreted by mast cells and basophils, cause edema and eosinophilic infiltration of the nasal mucosa and sometimes the conjunctiva of the eyes. Edema of the mucous membrane of the turbinates contributes to the stratification of a secondary infection and the development of sinusitis and edema.

Allergic (eosinophilic) bronchitis and bronchial asthma

The disease is characterized by the presence of cough, abundant secretion of bronchial secretions, containing a large number of eosinophils. Asthma (suffocation) is understood as an increased sensitivity of the bronchi to irritants, which leads to their spasms and labile obstruction.

Etiology . The main role in the development of allergic bronchitis and bronchial asthma is played by allergens - plant pollen, fungal spores, dust, smoke, volatile chemicals, some drugs, food products, and waste products of bacteria.

The predisposing factors are genetically determined instability of cell membranes, a violation of the relationship between the regulators of the immune system. Also influenced by low temperature and high humidity air.

Secondary bronchospasm is noted in chronic bronchitis, bronchopulmonary infection.

Pathogenesis the disease is caused by an allergic reaction of type I, sometimes type II.

Clinical picture . Clinical signs of the disease appear immediately after inhalation of the allergen. They are characterized by a suffocating cough, sneezing, expiratory shortness of breath, wheezing, conjunctivitis, and vomiting may occur. In the presence of bronchial asthma, there is a release of viscous mucus and edema of the bronchial mucosa, which leads to asthma attacks. Auscultation reveals wet and dry wheezing, whistling.

On an X-ray image, the lung has increased transparency, the diaphragm is flattened. In chronic cases, the bronchial tree is clearly expressed, interstitial and alveolar opacities are noted.

With the help of laboratory tests, an increased content of eosinophils in the blood and a large number of them in the bronchial secretions are found.

Food allergy

An immediate allergic reaction can develop to food.

Most often, allergies are caused by some animal proteins (milk, pork, fish, poultry) and flour products - oatmeal, wheat and other chicken eggs can also serve as food allergens.

Food allergies can occur locally and systemically. In the first case, only the alimentary canal is exposed. There is an edematous reaction on the oral mucosa. If allergenic food is swallowed, the mucous membrane of the esophagus and stomach swells, vomiting begins. With a systemic manifestation of food allergy, the response develops within a few minutes and can lead, along with damage to the alimentary canal, to an attack of bronchial asthma, angioedema and even anaphylactic shock. Hypersensitivity to allergenic foods can manifest as hives, swelling of the eyelids, tongue, and larynx.

Diagnosis of diseases, the pathogenesis of which is caused by allergies

Itype

Diagnostics of allergic pathologies includes the analysis of anamnestic data, clinical studies, examination of blood, sputum and other materials obtained from sick animals. Intradermal and contact tests are also performed. The results of the use of antihistamines have a certain diagnostic value. When analyzing anamnestic data, they find out which substances cause an allergic reaction. Pay attention to the dynamics of the pathological process. Type I allergy is characterized by the rapid appearance of clinical signs of the disease and their disappearance within 1-2 days after elimination of contact with the allergen.

The ineffectiveness of traditional treatment of inflammatory processes with the use of antimicrobial drugs and the positive effect of the use of antihistamines indicate the allergic nature of the disease.

Diseases, the pathogenesis of which is caused by type I allergy, are hyper-acute and acute. Their clinic is characterized by aseptic inflammation and edema of the skin, subcutaneous tissue, mucous membranes of the mouth, intestines and alimentary canal. At the same time, the same allergens, depending on the route of administration into the body and the dose, can cause both local lesions and anaphylactic shock. The greatest danger to the life of animals is anaphylactic shock, since it is accompanied by heart failure and pulmonary edema. In case of skin lesions, type I allergies are characterized by edema, itching, and urticaria.

When diagnosing allergies, identifying the allergen is key. For this purpose, intradermal and contact tests, or an oral test, are used.

Intradermal test ... The suspected allergen is administered intradermally in a volume of 0.1 or 0.05 ml. Before setting the sample, the hair is shaved, and the skin is treated with ethyl alcohol. The injected material must be sterile. For sterilization of thermolabile substances, bacteriological filters are used, thermostable substances are autoclaved.

A positive reaction with type I allergy is characterized by the formation of swelling and redness or blisters at the injection site of the allergen after a few minutes. These signs disappear without treatment in 24-48 hours.

Contact test is less sensitive. When it is set, a tampon moistened with the test substance is attached to the skin with a plaster. With a positive reaction, the skin at the site of contact with the allergen turns red after 1-2 hours.

Oral test ... When it is placed on the mucous membranes of the oral cavity, the allergen is applied in the form aerosols... The mucous membrane of the oral cavity swells and turns red 3-5 minutes after the oral test.

Laboratory research... Hematological studies can reveal eosinophilia in allergy sufferers. In animals with allergic bronchitis and asthma, microscopy of smears stained with azure-eosin in sputum reveals an accumulation of eosinophils.

Obtaining a positive result when using antihistamines has a certain diagnostic value.

Differential diagnosis is aimed at excluding diseases caused by viruses, bacteria, fungi, physical and chemical factors.

Treatment

First, it is necessary to exclude the entry of the allergen into the animal's body. Treatment is carried out in a comprehensive manner, with the use of drugs that affect all links of the pathological process and taking into account the clinical manifestation of the disease.

Prescribe drugs that inhibit the release of histamine, bradykinin, serotonin by mast cells and reduce the sensitivity of body cells to them.

In the presence of bronchial spasms, hypersecretion of bronchial glands and coronary insufficiency, which occurs with anaphylactic shock, allergic bronchitis and bronchial asthma, bronchodilators and drugs that block M-cholinergic receptors and stimulate α- and β-adrenergic receptors are also used.

The names of drugs and doses for different species of animals are shown in the table.

Doses of drugs for the treatment of allergies in different species of animals

Drug name	Release form	Methods of administration
Prednisolone is a synthetic glucocorticoid. It inhibits the degranulation of mast cells and basophils and the release of histamine, bradykinin, etc. into the blood.	tab. 0.001 and 0.005 g; amp. 3% - 1 ml		0.25-1 mg / kg IV, IM or oral; You can 600-800 mg (1.3-1.7 mg / kg) per animal weighing 450 kg / m or orally. Then reduce the dose to 0.4 mg / kg every other day (200 mg per animal) and until discontinuation.	1-4 mg / kg by mouth, IM or oral;	0.2-1 mg / kg i / v or i / m	0.2-1 mg / kg i / v or i / m	0.25-10 mg / kg orally or parenterally; To suppress the inflammatory process, the initial dose is 0.5-1 mg / kg 2 r / day peros. After 5-7 days, 1–2 mg / kg every other day orally and reduce dose until discontinued; Substitution treatment 0.25 mg / kg per day peros; In case of prednisolone allergy, succinate (water-soluble) 0.5-1 mg / kg 2 r / day i / v and i / m; In case of shock 5-10 mg / kg, repeat after 1, 3 and sometimes 6 hours.	1-4 mg / kg per day i.v., i.m. or orally, dividing the daily dose into 2 doses; Pulse therapy 50-100 mg / kg IV.
Dexamethasone is a synthetic long-acting glucocorticoid. Pronounced anti-inflammatory and anti-allergic action. 35 times more active than cortisone and 7 times more active than prednisone.	tab. 0.0005 and 0.001 g; amp. 4 mg 1 ml	B / articular	0.01-0.05 mg / kg 1 r / day i / v, i / m and orally; 5-20 mg per animal	0.01-0.05 mg / kg 1 r / day i / v, i / m, s / c and orally; 5-20 mg per animal	0.05-2 mg / kg i / m or i / v; 1-10 mg per animal	0.05-2 mg / kg i / m or i / v; 1-10 mg per animal; Piglets 0.5 mg	0.05-2 mg / kg; As anti-inflammatory - 0.05 mg / kg 1–2 r / day orally; In shock, cerebral edema 1-2-4 mg / kg IV, repeat after 4-6 hours. Then 0.5 mg / kg 2-3 r / day during the day. Further reduce the dose until discontinued; Topically (intrabursal) 2-4 mg 1 / once a day until 3 days	0.1-0.5 mg / kg i / v, s / c or i / m; Topically (intrabursal) 2-4 mg 1 / once a day until 3 days
Atropine sulfate. A drug that blocks m-cholinergic receptors and thus neutralizes the action of acetylcholine. Has an antispasmodic effect, reduces the tone of smooth muscles of the bronchi, intestines, bladder and suppresses the secretion of bronchial, nasopharyngeal and digestive glands	amp. 0.1% - 1 ml; table 0.005g; 1% eye ointment; eye films		0.04-0.15 mg / kg	0.04-0.15 mg / kg	0.1-0.15 mg / kg	0.1-0.15 mg / kg	0.2-1 mg / kg 1-2 r / day s / c; For premedication before anesthesia 0.02-0.05 mg / kg sc. i / m and i / v. with an increase in salivation, sinus bradycardia, the indicated dosage is repeated until the effect is achieved or orally 3 r / day; In case of poisoning with alkyl phosphate 0.2-2 mg / kg, ¼ dose i / v, the rest s / c or i / m	0.1-1 mg / kg s.c.
Epinephrine hydrochloride (epinephrine) is an analogue of endogenous catecholamine. The drug relaxes the smooth muscles of the bronchi and iris, antagonist histamine, enhances glycogenolysis, increases blood sugar, when administered intravenously, increases the heart rate, has a vasoconstrictor effect and increases systolic blood pressure. In veterinary practice, it is used for anaphylaxis, to stimulate the heart. With subcutaneous administration of the drug, the effect occurs later, after 5-10 minutes. When administered orally, it has no effect.	amp. 0.1% - 1 ml bottle 10 ml 0.1%			0.5-1 ml / 40 kg at a dilution of 1: 1000 s / c or i / m		0.5-3 ml / 50 kg at a dilution of 1: 1000 s / c or i / m		For anaphylaxis at a dilution of 1: 10000 at a dose of 0.01-0.02 mg / kg slowly intravenously, i / m or s.c., or intratracheally a double dose
Euphyllin is a myotropic bronchodilator. It causes a decrease in the intracellular concentration of calcium ions and relaxation of the muscles of the bronchi, reduces pressure in the pulmonary circulation, improves blood circulation in the heart, kidneys and brain.	amp 24% - 10 ml for i / m amp 2.4% - 10 ml for i.v.		1-4 mg / kg s.c.	1-4 mg / kg s.c.	4-6 mg / kg s.c.	4-6 mg / kg s.c.	Inside 25 mg / kg IM 25-50 mg / kg in 10-20 ml of 40% glucose solution; IV 2.5-5 mg / kg	S / c 3-5 mg / kg
Diphenhydramine is an antihistamine. Inhibits histamine at the H1 receptor sites. It has sedative, anticholinergic, anti-cough and antiemetic effects. In veterinary medicine, it is used as an antihistamine, for the treatment of itching, especially associated with allergic reactions, for the prevention of stress during the transportation of animals.	tab. 0.02; 0.03; 0.05g; amp. 1% - 1 ml	n / a, inside, topically (cutaneous, in the form of eye drops, on the next page)	0.25-1 mg / kg i / v or i / m	0.5-1 mg / kg i / v or i / m	0.5-0.6 mg / kg	0.5-0.6 mg / kg	2-4 mg / kg i.m.	2-4 mg / kg i.m.
amp 1% - 1 ml	Doses inside 1.5-2 times more

It should be noted that the use of the above drugs makes it possible to transfer the disease from the acute stage to the remission stage. It does not eliminate etiological factors and does not exclude, in case of repeated contact with allergens, the manifestation of the disease in an acute form.

Persistent remission can be obtained with the complete exclusion of the animal's contact with the allergen or a decrease in the body's sensitivity to the latter.

In order to reduce the sensitivity of the animal's body to the allergen, the method of hyposensitization is used. When it is performed, first, using intradermal tests, it is determined which substance is an allergen for the animal. Then the specified substance in small doses for a long time is introduced into the animal's body parenterally.

This method gives positive results in the presence of 1-2 allergens. With multiple allergies, when a large number of different substances are allergens, it is ineffective.

Prophylaxis Allergies include compliance with sanitary and hygienic requirements in keeping animals, selection work, timely and effective treatment of diseases, exclusion from the diet of substances that exhibit allergenic properties.

For the prevention of drug allergies, the method of fractional administration is used (desensitization according to Bezredko). When using this method, first, 1/10 of the dose of the drug is administered to the animal, then, after 1.5-2 hours, the remaining 9/10 parts are administered. This method eliminates the clinical manifestation of an allergic reaction.

Autoimmune reactions

Autoimmune reactions are characterized by the formation of antibodies or sensitized lymphocytes to the body's own antigens. The pathogenesis of these reactions develops according to type II allergy. Currently, there are several reasons for the appearance of autoimmunity.

One of them is the release of "hidden" antigens, that is, antigens that are isolated from immunocompetent cells by blood-tissue barriers. In particular, "hidden" antigens are internal components of cells, vitreous body, pancreatic parenchyma, testis tissue, brain, thyroid gland. When the blood-tissue barriers are damaged, "hidden" antigens are released and trigger the body's immune response. For example, when the emulsified tissue of the previously removed testis is parenterally administered to the host, damage to the tissues of the healthy testis occurs after a while. The autoimmune reaction also explains sympathetic ophthalmia, which is observed in a healthy eye with a penetrating injury to the other eye.

Autoantigens can be formed in the body as a result of protein denaturation by physical, chemical or biological factors. Such denaturation can be observed as a result of burns, frostbite of tissue, exposure to drugs and microbial toxins.

Autoimmune reactions can occur when antigens that are similar to tissue proteins of a macroorganism are introduced into the body. For example, it was found that in the blood serum of animals with abscesses caused by corynebacteria, antibodies to bovine hemoglobin are present. Also found similar properties in antigens of streptococcus, myofibrils of the heart and kidney tissue. The properties of autoantigens can be possessed by complex compounds that are formed when proteins of a macroorganism combine with the waste products of microorganisms.

Autoimmune processes are more common in old age, since with aging there is an accumulation of mutant forms of somatic cells.

And, finally, the cause of autoimmune reactions can be a deficiency of the immune system, namely, a violation of its ability to identify its own antigens from foreign ones. It is believed that one of the reasons for this deficiency is a deficiency of various forms of T - and B-lymphocytes.

Autoimmune processes play a role in the pathogenesis of autoimmune hemolytic anemia, hepatitis, pancreatitis, gastritis, myocarditis, rheumatic arthritis, systemic lupus erythematosus, etc.

For diseases in the pathogenesis of which the autoimmune component is involved, eosinophilia, accelerated ESR, is characteristic. In the blood serum, antibodies to its own antigens and C-reactive protein are found.

For the treatment of animals with the above diseases, along with other necessary drugs, it is recommended to use glucocorticosteroids, cytostatics and other immunosuppressants.

Autoimmune hemolytic anemia

The disease is characterized by severe anemia, splenomegaly, swollen lymph nodes, jaundice. Described in dogs and cats, females are more often sick.

Etiology ... The main etiological factor is a change in the antigenic structure of the cell wall of erythrocytes, as a result of which they acquire the properties of autoantigens.

Pathogenesis ... Erythrocyte wall autoantigens induce the production of autoantibodies of the IgM and IgG classes to them.

Antibodies form immune complexes (AG-AT) with erythrocytes, which cause the classical activation of the complement system. The 8th and 9th components of the complement system have lytic properties. They cause lysis of red blood cells. In the process of hemolysis, macrophages of the spleen and lymph nodes are also involved. As a result of massive hemolysis, a large amount of free hemoglobin is released. Part of it is converted by phagocytes of the liver and lymph nodes into free bilirubin, and part is excreted in the urine.

Clinical picture ... Animals are depressed, there is shortness of breath, anorexia, vomiting, fever. Due to severe anemia, the mucous membranes have a porcelain appearance, the spleen and peripheral lymph nodes are greatly enlarged in size. There is a yellowness of the sclera, the urine is dark brown, the feces are dark. The heart rate is increased. There is blood in the anterior chamber of the eye (black eye).

In laboratory blood tests, severe anemia is revealed, the concentration of erythrocytes decreases to 1-2 x1012 / l, the osmotic resistance of erythrocytes is reduced. Spherical erythrocytes (spherocytes) and reticulocytes are found.

With the help of immunological tests on the surface of erythrocytes, immunoglobulins G and M classes and C3 (the third component of complement) are detected.

Diagnostic the presence of anemia, an increase in the size of the spleen and lymph nodes, the detection of spherical erythrocytes and IgM, IgG and C3 on erythrocytes is important.

Treatment Autoimmune hemolytic anemia aims to suppress the body's immune responses. To reduce phagocytic activity and inhibition of antibody synthesis, prednisolone is prescribed at the rate of 1 mg / kg of body weight 2 times a day. After seven days of treatment, the dose of prednisolone is continuously reduced until it is completely canceled. In some cases, sick animals must take prednisolone throughout their life at the rate of 0.5 mg / kg of body weight every three days. In cases where the use of glucocorticoids is insufficiently prescribed cytostatics. It is recommended to use cyclophosphamide at a dose of 1.5 mg / kg for dogs weighing more than 25 kg; 2.0 mg / kg for animals weighing 6-24 kg; 2.5 mg / kg - for animals weighing less than 5 kg. The drug is taken orally 4 times a week for three weeks.

If there are signs of oxygen deficiency, oxygen therapy is performed.

Prophylaxis the disease is aimed at eliminating etiological factors. It is necessary to timely treat infectious, invasive and non-communicable diseases, to exclude from the use of drugs that cause damage to erythrocytes. Animals with autoimmune anemia are excluded from breeding.

Autoimmune atrophic gastritis

This is a rare disease characterized by atrophy of the gastric mucosa and loss of secretory capacity.

Etiology ... Autoimmune gastritis has been linked to a genetic predisposition. Older dogs are more likely to get sick. Autoimmune processes underlie atrophic gastritis (Twedt & Magne, 1986). The body produces antibodies that damage the main, accessory and lining cells of the fundic glands of the stomach with their subsequent loss.

Pathogenesis ... In this disease, mucosal atrophy occurs, which leads to a decrease in the number of acid-producing cells. As a result, the volume of gastric juice and hydrochloric acid decreases. The pH level rises above 3.5. All of these can lead to overgrowth of small intestinal microflora, poor absorption, chronic diarrhea, and weight loss.

Clinical picture ... Atrophic gastritis is characterized by chronic intermittent vomiting, often over several months. The vomit contains mucus, bile, and pieces of undigested food. Belching and anorexia are possible, sometimes abdominal pain (the position of the prayer).

Diagnosis ... Gastroscopy reveals thinning of the mucous membrane with a small number of uneven flattened crestal folds, an increased content of mucus in the lumen of the stomach. The blood vessels of the submucosal layer are clearly visible.

A mucosal biopsy provides important information. Loss of glandular tissue, infiltration of plasma cells, and various degrees of fibrosis are observed microscopically.

An X-ray can provide additional information. Autoimmune atrophic gastritis must be differentiated from secondary atrophic gastritis, a tumor.

Forecast careful. Complete recovery usually does not occur. Chronic atrophic gastritis is referred to as precancerous conditions of the stomach, against the background of this disease, such precancerous changes as intestinal metaplasia and dysplasia of the epithelium of the gastric mucosa, as well as hyperproliferation of the epithelium of the gastric mucosa, which contribute to the development of tumors, often develop.

Treatment ... A gentle diet is required. Feeding should be frequent, in small portions. Preferably meat, not porridge, it is better to choose a diet hypoallergenic. Dry food can drown the symptoms of the disease for a while, since they do not require a large amount of gastric juice and are easily digested.

If necessary, prescribe preparations of gastric juice (pepsin, hydrochloric acid). Antibiotics may be necessary in case of excessive development of pathogenic microflora and chronic diarrhea. Tylosin is prescribed at 20 mg / kg of live weight 2 times a day.

Glucocorticoids are prescribed with caution. Although they suppress the autoimmune process, they can also cause stomach ulcers by stimulating the production of hydrochloric acid. Azathioprine is recommended.

Chronic active hepatitis

It is a progressive autoimmune disease characterized by focal necrosis of hepatocytes in the limiting plate of the acinus.

Clinical picture ... Apathy, anorexia, mild jaundice, weakness. Later, polyuria, polydipsia, jaundice, emaciation, melena and vomiting appear. Ultimately, portal hypertension, ascites, cirrhosis or liver fibrosis, and hepatoencephalopathy develop.

Diagnosis ... To make a diagnosis, it is necessary to conduct biochemical blood serum tests. A strong, 15-fold increase in the level of serum alanine aminotransferase, as well as alkaline phosphatase, bilirubin is observed. The clearance of bromsulfophthalein is reduced. Hypergammaglobulinemia and hypoalbuminemia are also characteristic.

Differential diagnosis is carried out with chronic progressive hepatitis. Unlike chronic active hepatitis, it is a relatively benign hepatitis, with a slight tendency towards cirrhosis or fibrosis, which can heal spontaneously. In contrast, chronic active hepatitis often leads to liver failure and death. For differential diagnostics is necessary biopsy as the liver may appear to be unchanged macroscopically. The presence of periportal necrosis, as well as a significant increase in the level of transferases, hypergammaglobulinemia, and unsuccessful therapy confirm the diagnosis of chronic active hepatitis. You also need to differentiate the disease from chronic cholangitis, liver granules, copper storage disease (in Bedlington Terriers, Dobermans).

Forecast doubtful.

Treatment ... Diet and multivitamins are essential. After clinical improvement, glucocorticoids are prescribed. Prednisolone is used at a dose of 1–2 mg / kg with a gradual dose reduction after clinical improvement. It can be combined with azathioprine at a dose of 1 mg / kg.

Cats have chronic cholangiohepatitis caused by immune-mediated factors. The course of the disease resembles primary biliary cirrhosis. The initial bacterial infection is thought to cause an immune-mediated hepatocellular lesion or destruction of the bile duct that exacerbates the initial lesion. Clinical signs of the disease are similar to those found in acute cholangiohepatitis (anorexia, weight loss, weakness, drowsiness, vomiting, often hepatomegaly, sometimes fever). In the blood, neutrophilia is observed with a shift of the nucleus to the left. Biochemical disorders include an increase in the concentration of total bilirubin.

Treatment ... Prescribe ursodeoxycholic acid at 10-15 mg / kg orally once a day. Prednisolone 2.2-6.6 mg / kg once a day with a gradual dose reduction to 2-4 mg / kg once every two days as a long-term maintenance therapy.

Autoimmune pancreatitis

Autoimmune pancreatitis is an inflammation of the pancreas, which is based on the production of antibodies against its own pancreatic tissue. Dogs suffer from acute pancreatitis more often than cats.

Etiology ... The same causes that cause non-immune pancreatitis can lead to the production of autoantibodies. This is a diet saturated with fats, mechanical injury, drugs (sulfamethasole, azathioprine, corticosteroids, furosemide, chlorothiazide, estrogens, sulfonamides). Cushing's syndrome results in high levels of cortisol in the blood, which causes acute pancreatitis. In cats, pancreatitis may occur after treatment with tetracycline drugs. Pancreatitis can be caused by infectious agents (parvovirus, toxoplasma, etc.). The relationship between hyperlipidemia, hypercalcemia and hypovolemia with the development of pancreatitis has been established. These phenomena can cause organ ischemia, activate and increase the production of enzymes by the pancreas.

Pathogenesis ... The basis of the pathogenesis of autoimmune pancreatitis is a change in the antigenic structure of pancreatic cells caused by physical, chemical, mechanical, biological and other factors. The body produces antibodies against cells with altered antigenic structure. Antibodies form an antigen-antibody complex with altered cells, which activates the complement system, the 8th and 9th components of which have lytic activity. Cytolysis of the tissue is noted. At the same time, pancreatic enzymes are activated, in particular trypsin. Trypsin activates two other enzymes. It is elastase, which breaks down the elastic fibers of blood vessels, leading to bleeding, thrombosis and ischemia, and, in addition, digests interstitial connective tissue. The second enzyme is phospholipase A, which breaks down acinar cell membranes, which enhances the release of enzymes. Acute inflammation and pain begin, leading to hypovolemia and shock. Trypsin also activates bradykininogen, which ultimately leads to extensive circulatory collapse. The release of lipase leads to fatty necrosis.

Against the background of hypovolemia and ischemia of the pancreas, Clostridia microorganisms begin to multiply, which can lead to peritonitis.

The possible end result of an acute form of the disease is irreversible shock and disseminated intravascular coagulation. In the chronic form of pancreatitis, the inflammatory process gradually leads to the complete replacement of exocrine tissue with fibrous tissue, which is manifested by exocrine pancreatic insufficiency and the development of diabetes mellitus.

Clinical picture ... Autoimmune pancreatitis is usually difficult. Anorexia, depression, dehydration, abdominal pain, and vomiting are observed. The feces are frequent and profuse, with a sour odor, diarrhea is possible. Intestinal peristalsis is enhanced, it is swollen. Jaundice is common in cats because they share a common pathway for bile and pancreatic secretions. At the beginning of the disease, there may be an increase in temperature up to 40 ° C, and then, as the shock develops, on the contrary, a drop in body temperature.

In addition to the signs described above, hypocalcium tetany, shortness of breath, cyanosis, pulmonary edema, hyperglycemia, hemorrhagic diathesis, blood in the feces and vomit (signs of DIC syndrome) may be observed.

In the chronic form of pancreatitis, despite the fact that the animal eats, it loses weight, owners complain of dull coat and persistent shedding.

Diagnosis ... The disease must be differentiated from an abscess, from hemorrhagic gastroenteritis, hepatitis, intestinal perforation, acute gastritis.

Hematological analysis reveals an increase in the hematocrit value (a consequence of dehydration), neutrophilic leukocytosis with a shift of the nucleus to the left. An increase in serum amylase and lipase levels may indicate liver and kidney disease, that is, it does not always indicate the presence of pancreatitis. Nevertheless, a threefold excess of the physiological values ​​of these indicators is certainly significant. A large amount of amylase and lipase is also found in the ascites fluid.

When examining feces, a large number of fat drops are noted, which indicates a violation of the digestion of fats. On ultrasound, the pancreas is diffusely enlarged, has an irregular shape, and mixed echogenicity. Two days before the study, special attention should be paid to the prevention of gas formation, since in animals with pancreatitis, the intestines are swollen. On the roentgenogram (it is desirable to conduct a study with contrast) darkening in the right hypochondrium, ventral or right-sided displacement of the duodenum, displacement in the caudal direction of transversely located sections of the colon.

Forecast with edematous pancreatitis, which is more common in cats, favorable or cautious. In acute necrotizing pancreatitis, the prognosis is dubious.

Treatment ... To prevent hypovolemia and metabolic acidosis, a 5% sodium bicarbonate solution or Ringer's solution is administered intravenously. To neutralize lipase in the blood, counterkal is prescribed. When vomiting - metoclopramide hydrochloride (raglan) intramuscularly or subcutaneously at a dose of 0.2-0.4 mg / kg every 6-8 hours (R. Kirk. D. Bonagura, 2005).

To reduce further secretion of pancreatic enzymes, it is important to stop eating in the first 2-5 days. When appetite appears, parenteral or enteral nutrition is prescribed. To suppress pancreatic secretion, anticholinergic drugs (sulfate atropine), intravenous glucagon at a dose of 0.3 mg / kg, intravenous insulin at a dose of 0.5 IU / kg (J. Simpson, 2003). Enzyme preparations (Creon, Panzinorm) are prescribed.

To stop the development of primary and secondary infection, antibiotics of a wide spectrum of action are always prescribed, such as gentamicin, ampicillin, amoxicillin, chloramphenicol (J. Simpson, 2003), or baytril, which penetrates well into the tissue of the pancreas, intramuscularly at a dose of 2.5 mg / kg every 12 hours for dogs (R. Kirk. D. Bonagura, 2005).

Corticosteroids are used with great caution. They themselves can cause acute pancreatitis. They should be used only for conditions close to shock, for example, prednisone at a dose of 6-10 mg / kg. To relieve pain, antispasmodics can be used - no-shpu, papaverine, baralgin, or analgesics, for example, butorphanol at a dose of 0.2-0.4 mg / kg every 6 hours subcutaneously in dogs and cats (R. Kirk. D. Bonagura, 2005 ).

In the initial stages of the disease, a diet high in carbohydrates (boiled rice) and low in fat and protein is required.

Diseases of the immune complexes

The pathogenesis of diseases of the immune complexes is associated with an allergic reaction of type III. The formation of immune complexes consisting of precipitating antibodies of the IgG and IgM classes and antigens in quantities exceeding the body's ability to metabolize them is noted with the use of hyperimmune serum, hyperimmunization of the body, and chronic diseases.

Of the diseases of immune complexes, glomerulonephritis, serum sickness, Arthus phenomenon and rheumatoid arthritis are of the greatest practical importance in veterinary practice.

Glomerulonephritis

This is inflammation of the renal glomeruli, which is caused by immune complexes and antibodies. The disease is characterized by the manifestation of hypersensitivity in the vascular glomeruli of the kidneys, proliferation of the endothelium and thickening of their capillary membranes. Glomerulonephritis has an acute and chronic course.

Etiology ... The disease is more often of an infectious-allergic nature, less often it is not associated with infectious agents. In animals, glomerulonephritis occurs after previous infectious diseases, immunization, or the use of hyperimmune serum and specific immunoglobulins; can develop as a result of chronic uroinfection, pustular skin lesions, with purulent sinusitis, sinusitis caused by streptococci and staphylococci.

The cause of the disease can be drugs, especially some antibiotics and vitamins, toxins of organic and inorganic origin, pollen. Adverse environmental factors - low temperature and high air humidity - contribute to the disease of animals with glomerulonephritis. There is information about the genetic predisposition of animals to glomerulonephritis disease.

Pathogenesis ... The pathogenetic basis of glomerulonephritis is an allergic reaction of type III. The leading role in its development is attributed to immune reactions that develop on the basement membrane of the capillaries of the renal glomeruli with the participation of circulating immune complexes. In some cases, autoantibodies to kidney tissue play this role.

The formation of complexes of antigen and antibodies is normal. Subsequently, these complexes are metabolized by mononuclear phagocytes. When an excessive amount of antigen enters the body, part of the formed complexes is deposited on the basement membrane of the capillaries. Immune complexes activate the complement system. In this case, the fifth and third components of the complement system after activation (C5 and C3) acquire chemotactic properties. They attract neutrophils to the lesion and stimulate phagocytosis. The enzymes released from the lysosomes of neutrophils during phagocytosis damage the basement membrane of the capillaries of the renal glomeruli. As a result of membrane damage, erythrocytes and plasma proteins appear in the urine, blood coagulates in the capillaries, and platelet aggregation is noted.

In the chronic course of glomerulonephritis morphological changes in the glomeruli can be characterized by sclerosis of individual capillaries, massive deposition of immune complexes on their basement membranes, proliferation of mesangial cells with their penetration into the lumen of the capillaries.

Clinical picture ... Symptoms of glomerulonephritis appear 12-14 days after immunization of those who have had an infectious disease or exposure to other etiological factors. The disease can occur in two forms - cyclic and latent.

The cyclical form develops rapidly and proceeds violently. There is general depression, refusal to feed, body temperature can increase by 1-1.50C, kidney area on palpation and percussion painful... For the cyclic form of glomerulonephritis, urinary, edematous and hypertensive, nephrotic syndromes are characteristic. The urine takes on the color of meat slops, its density is lowered.

In laboratory tests of urine, hematuria, proteinuria, the presence of hyaline and erythrocytic casts are noted. Hematological parameters are characterized by leukocytosis, accelerated ESR.

In the blood serum, the content of urea, creatinine, cholesterol is increased, the alkaline reserve is lowered, clearance endogenous creatinine is lowered.

With a favorable course of the disease and effective treatment, these symptoms disappear after 2-3 weeks. If untreated, the disease can take on a chronic course.

With a latent form, glomerulonephritis occurs without pronounced clinical signs. Nephrotic and hypertensive syndromes are absent. Clinically, the disease is manifested by slight shortness of breath and edema. Urinary syndrome is poorly expressed, it is characterized by nocturia and microhematuria.

The latent form of acute glomerulonephritis in the absence of rational treatment often turns into chronic glomerulonephritis.

Under the influence of unfavorable environmental factors, in particular stress, low temperatures and high humidity, which lead to a decrease in the natural resistance of the body, chronic glomerulonephritis can worsen. Especially often exacerbations are observed in autumn and spring.

Chronic glomerulonephritis ends with a secondary wrinkled kidney.

Diagnostics cyclic glomerulonephritis is carried out in a complex manner. The appearance of signs of the disease 12-14 days after an infectious disease or immunization, the use of hyperimmune serum, as well as severe hematuria are of diagnostic value. The disease develops acutely and is characterized by soreness and enlargement of the kidneys. Urine has the color of meat slops, the content of erythrocytes in it prevails over the number of leukocytes. Acute renal failure, uremic and nephrotic syndromes are noted. The echogram shows the expansion of the cortical layer and a decrease in its echogenicity. Puncture biopsy of the kidneys in animals with glomerulonephritis shows an increase in the size of the glomeruli (80-100%), a narrowing of the lumen of their capillaries, an increase in the thickness of the mesangial matrix, and an abundance of neutrophilic leukocytes. Along the basement membranes of the glomerular capillaries and in the mesangia, using special test systems, granular lumpy deposits are found, consisting of immunoglobulins of class G and C3 (the third component of complement).

The latent form is characterized by the absence of pronounced clinical signs, proteinuria, microhematuria, and the presence of edema.

In chronic course, the echogenicity of the cortical layer increases.

Treatment glomerulonephritis is aimed at eliminating contact with antigens, suppressing microorganisms and an allergic inflammatory reaction in the renal glomeruli, and stimulating diuresis.

To suppress microflora, antibiotics, sulfa drugs, nitrofurans, quinolones, fluorochtolones are used. Preference is given to active, non-nephrotoxic drugs that are excreted from the body unchanged by the kidneys.

From antibiotics, claforan, ampiox, chloramphenicol, tetracycline are used, from nitrofuran compounds - furadonin and furagin, from the group of quinolones - nitroxoline (5-NOK), from fluoroquinolones - norfloxacin (nolicin).

To suppress the inflammatory allergic reaction, prednisolone or dexamethasone and drugs that have an immunosuppressive effect (cyclophosphamide) are prescribed. Diuresis is stimulated with furosemide.

Serum sickness

Serum sickness is caused by immune complexes and is characterized by high fever, urticaria, lymphadenitis, arthritis, glomerulonephritis, heart failure.

Etiology ... Serum sickness develops 8-14 days after the introduction of large doses of foreign hyperimmune serum or other protein preparations to animals.

Pathogenesis serum sickness develops according to the III type of allergic reaction, that is, with the participation of immune complexes. When a large amount of a heterogeneous protein is introduced into the body, the synthesis of antibodies to it begins earlier than the metabolism and elimination of the drug from the body occurs. Antibodies form immune complexes with the remnants of a foreign protein. Immune complexes, especially those consisting of positively charged proteins and antibodies, are deposited on the basement membranes of the capillaries of the renal glomeruli, synovium, skin, choroid of the eyeball.

Later, as in glomerulonephritis, complement is activated with the formation of C5 and C3, chemotaxis of neutrophils, phagocytosis with the release of lysosomal enzymes that damage the basement membranes of capillaries.

Damage to the basement membranes of the capillaries is accompanied by the development of an aseptic inflammatory response.

Clinical picture ... The clinical picture of serum sickness is characterized by high fever, urticaria, glomerulonephritis, arthritis, uveitis, pericarditis, inflammation of the lymph nodes, heart failure. Inflammatory processes develop aseptically.

Diagnostics ... When diagnosing, anamnestic data on the use of hyperimmune serum or other protein preparations in a sick animal 8-14 days before the manifestation of clinical signs of the disease are important. The diagnosis is confirmed by the detection of the deposition of immune complexes in biopsy specimens.

Treatment ... In the treatment of serum sickness, antihistamines and anti-inflammatory drugs (diphenhydramine, prednisolone, dexamethasone) are used. They also carry out symptomatic treatment with the use of diuretics and cardiac drugs.

The Arthus Phenomenon

The disease is a model of local damage to body tissues by immune complexes. It develops after intradermal administration of a homologous antigen to a sensitized animal. The Artyus phenomenon is noted with hyperimmunization of experimental animals, with reimmunization against infectious diseases, as well as with bites by blood-sucking insects.

Clinical picture The Artyus phenomenon is characterized by the development within an hour at the site of intradermal, sometimes intramuscular injection of the antigen of exudative hemorrhagic inflammation. In the future, the foci of inflammation are encapsulated and turn into nodules, which undergo necrosis and lysis.

Pathogenesis diseases are associated with the formation of immune complexes in the walls of small vessels, fixation and activation of complement, and chemotaxis of neutrophils and monocytes. Lysis of damaged tissues is carried out by lysosomal enzymes of phagocytes.

Rheumatoid arthritis

Rheumatoid arthritis is a systemic allergic disease of the joints, characterized by the proliferation of synovial tissue and erosive-destructive damage to cartilage and ligaments.

Etiology ... Currently, the main role in the development of rheumatoid arthritis is assigned to immune complexes. The rheumatoid factor plays an important role in the formation of immune complexes. The rheumatoid factor, according to modern concepts, are class M autoantibodies to the Fc fragment of the host IgG. The formation of antibodies to their own immunoglobulins is explained by the presence of partial denaturation of the latter.

Hypothermia, hyperinsolation, intoxication, diseases of the endocrine system, stress contribute to the development of the disease. The hereditary predisposition of animals to rheumatoid arthritis has also been established.

Pathogenesis the disease is mainly caused by an allergic reaction of type III. Immune complexes are formed as a result of the binding of rheumatic factor (autoantibodies of class M) to immunoglobulins of class G of the host.

Rheumatoid factor is found in 20% of affected dogs. In some animals, autoantibodies to collagen and cartilage tissue were also found, which indicates changes in the structure of these tissues.

The reasons for the change in the structure of the body's own tissues have not been precisely established. It is believed that cell damage can be caused by bacteria and viruses. Immune complexes activate complement, C5 and C3 components of which have a chemotactic effect. It stimulates chemotaxis and lytic activity of phagocytes. Lysosomal enzymes - collagenase, neutral proteinase, as well as interleukin 1 and prostaglandins E1 cause an acute inflammatory reaction of the cells of the synovial lining, their increased division, as well as damage to cartilage and bone tissue.

Clinical picture ... Dogs of all ages and all breeds get sick, clinical signs of rheumatoid arthritis usually appear in cold, wet weather, with a change in atmospheric pressure, before rain, after heavy physical exertion, during the period of hormonal changes in the body, after viral and bacterial infections.

They are characterized by a symmetrical lesion at first of small, and then of large joints. The disease often proceeds slowly with the constant development of the clinical picture, less often it has an acute course. Initially, the joints of the distal parts of the limbs are affected. The disease can occur in the form of mono or polyarthritis.

Joint syndrome is characterized by stiffness after rest, swelling and tenderness of the joints with active movement. There is a general depression and refusal to feed, with an acute course, an increase in body temperature.

X-ray studies indicate the presence of periarticular tissue edema, infiltration of soft tissues. With erosive polyarthritis, exostoses, ankylosis, dislocations and subluxations are observed.

The detection of rheumatoid factor in blood serum using the Waaler-Rose test is rarely used in veterinary practice due to its low efficiency.

The diagnosis is made on the basis of the results of clinical, radiological and laboratory tests.

Rheumatoid arthritis must be differentiated from other types of disease not associated with immune complexes (infectious arthritis, drug arthritis, etc.)

Treatment rheumatoid arthritis aims to suppress the body's immune response.

Give prednisolone 2-4 mg / kg daily until improvement occurs. In the future, the dose of prednisolone is reduced to the minimum effective. In combination with prednisolone, acetylsalicylic acid is prescribed at the rate of 10-20 mg / kg per day.

In severe cases, cytostatic drugs are included in the treatment regimen. Dogs are advised to use the cytostatic cyclophosphamide. For animals weighing up to 10 kg, cyclophosphamide is prescribed at a dose of 2.5 mg / kg per day. For dogs weighing 10-35 kg, the drug is used at the rate of 2.0 mg / kg, for dogs weighing more than 35 kg - 1.5 mg / kg.

The drug is used 4 days a week for up to 4 months.

With a decrease in the concentration of leukocytes in the blood of a sick animal below 6x109 / l, the dose of cyclophosphamide decreases by 25%, and at a concentration below 4x109 / l, the dose is reduced by 50%.

Immunological tolerance

The lack of an immune response to antigenic irritation is called tolerance.

Tolerance in relation to antigens of one's own tissues is the main mechanism that prevents their immune damage.

Violation of the mechanisms of recognition of their own antigens leads to the development of autoimmune reactions.

Tolerance of the body's immune system in relation to antigens of vaccine strains of microorganisms is the reason for ineffective immunization.

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