Text of the article and photo 1-44 from the book SMALL ANIMAL DERMATOLOGY A COLOR ATLAS AND THERAPEUTIC GUIDE

KEITH A. HNILICA, DVM, MS, DACVD, MBA Copyright © 2011

Translation from English: veterinarian Vasiliev AB

Peculiarities

Pemphigus foliaceus in dogs and cats is an autoimmune skin disease characterized by the production of autoantibodies against a component of adhesion molecules on keratinocytes. The deposition of antibodies in intercellular spaces causes cells to detach from each other within the upper layers of the epidermis (acantholysis). Pemphigus foliaceus is probably the most common autoimmune skin disease in dogs and cats. Animals of any age, sex, or breed may be affected, but Akita and Chow Chow dogs may be predisposed among dogs. Pemphigus foliaceus in cats and dogs is usually an idiopathic disease, but in some cases it can be caused by drugs or may occur as a consequence of a chronic skin disease.

Primary lesions are superficial. However, intact pustules are often difficult to find because they are covered with hair, have a fragile wall and are easily torn. Secondary lesions include superficial erosions, crusts, scales, epidermal collars, and alopecia. Lesions of the nasal planum, auricles, and pads of the fingers are unique and characteristic of an autoimmune skin disease. The disease often begins on the back of the nose, around the eyes and on auricles before it becomes generalized. Nasal depigmentation is often associated with facial skin lesions. Skin lesions have variable itching and their severity may weaken or intensify. Finger pad hyperkeratosis is common and may be the only symptom in some dogs and cats. Oral lesions are rare. Mucosal junctions in dogs are minimally involved in the process. In cats, lesions around the nail bed and nipples are a unique and common feature of pemphigus. With generalized skin lesions, lymphadenomegaly, swelling of the extremities, fever, anorexia and depression can occur simultaneously.

Differential diagnosis of pemphigus foliaceus in dogs and cats

Includes demodicosis, superficial pyoderma, dermatophytosis, other autoimmune skin diseases, subcorneal pustular dermatosis, eosinophilic pustulosis, drug dermatosis, dermatomyositis, cutaneous epitheliotropic lymphoma, and

Diagnosis

1 Rule out other differential diagnoses

2 Cytology (pustules): neutrophils and acantholytic cells are visible. Eosinophils may also be present.

3 Antinuclear antibodies (ANA): negative, but false positives are common

4 Dermatohistopathology: subcorneal pustules containing neutrophils and acantholytic cells, with varying numbers of eosinophils.

5 Immunofluorescence or immunohistochemistry (skin biopsy specimens): Detection of intracellular antibody deposition is characteristic, but false positive and false negative results are common. Positive results must be confirmed histologically.

6 Bacterial culture (pustule): usually sterile, but sometimes bacteria are detected if secondary infection is present.

Treatment and prognosis

1. Symptomatic therapy shampoos to remove crusts can be helpful.

2. To treat or prevent secondary pyoderma in dogs, an appropriate long-term systemic antibiotic therapy(minimum 4 weeks). Dogs that were treated with antibiotics during the run-in phase of immunosuppressive therapy had significantly more time survival than dogs treated with immunosuppressive drugs alone. Antibiotic therapy should be continued until immunosuppressive therapy has brought pemphigus under control.

3. The goal of treatment is to control the disease and its symptoms in the least dangerous drugs used in the lowest possible doses. Typically, a combination therapy (see ) should be used that will minimize the side effects of any monotherapy. Depending on the severity of the disease, more or less aggressive drugs are selected for treatment. To obtain remission, higher doses are initially used, which are then reduced over 2-3 months to the lowest effective dose.

• .Topical treatment applied 2 times a day, in the form of steroid-containing drugs or tacrolimus will help reduce focal inflammation and allow dose reduction systemic drugs required to control symptoms. Once remission is achieved, the frequency of drug use should be minimized to reduce local side effects.
• . Conservative systemic treatment (see Table) includes drugs that help reduce inflammation with few or no side effects. These drugs help reduce the need for more aggressive therapies such as steroids or chemotherapy drugs.
• Steroid therapy is one of the most reliable and predictable treatments for autoimmune skin diseases; however, side effects associated with high doses needed to control symptoms can be severe. Although glucocorticoid therapy alone may be effective in maintaining remission, the required doses may lead to undesirable side effects, especially in dogs. For this reason, the use of non-steroidal immunosuppressive drugs, alone or in combination with glucocorticosteroids, is usually recommended for long-term maintenance treatment.

Immunosuppressive doses of oral prednisolone or methylprednisolone should be given daily (see Table). After the lesions resolve (after approximately 2-8 weeks), the dose should be tapered gradually over several (8-10) weeks to the lowest possible dose given every other day that supports remission. If there is no significant improvement within 2-4 weeks of starting treatment, a concurrent skin infection should be ruled out and then alternative or additional immunosuppressive drugs should be considered. Alternative steroids in cases refractory to prednisolone and methylprednisolone include triamcinolone and dexamethasone (see Table)

In cats, treatment with immunosuppressive doses of triamcinolone or dexamethasone is often more effective than therapy with prednisolone or methylprednisolone. Oral triamcinolone or dexamethasone should be given daily until remission (approximately 2-8 weeks), then the dose should be reduced to the least possible and least frequent that maintains remission (see Table). If unacceptable side effects develop or if significant improvement is not achieved within 2-4 weeks of starting treatment, consider using alternative glucocorticosteroids or non-steroidal immunosuppressive drugs (see Table).

• . Non-steroidal immunosuppressive drugs that may be effective include cyclosporine (Atopica), azathioprine (dogs only), chlorambucil, cyclophosphamide, mycophenolate mofetil, and lefunomide (see Table). A positive effect is observed within 8-12 weeks after the start of treatment. Once remission is achieved, gradually try to reduce the dose and frequency of non-steroidal immunosuppressive drugs for long-term maintenance treatment.

4 Prognosis is cautious to good. Although some animals remain in remission after immunosuppressive therapy is tapered off and withdrawn, most animals require lifelong treatment to maintain remission. Regular monitoring required clinical symptoms, blood tests with treatment adjustments as needed. Potential complications of immunosuppressive therapy include unacceptable side effects medicines and immunosuppression-induced bacterial infections, dermatophytosis or demodicosis.

Photo 1 Pemphigus foliaceus in dogs. Adult Doberman with pemphigus foliaceus. Note the diffuse nature of the lesions.

Photo 2. Pemphigus foliaceus in dogs. Same dog in photo 1. Alopecia, crusting and papular lesions on the muzzle are evident. Note the similarity of lesions to folliculitis: however, the pattern of distribution of lesions is unique.

Photo 3. Pemphigus foliaceus in dogs. Alopecia, crusting, papular dermatitis on the face. Lesions of the nasal planum and auricles are characteristic of an autoimmune skin disease.

Photo 4. Pemphigus foliaceus in dogs. The same dog from photo 3. Alopecia, crusting, papular dermatitis on the face and nasal planum are characteristic of an autoimmune skin disease. Note the similarity of the lesions to folliculitis; however, follicles are absent from the nasal planum, making these lesions a unique feature.

Photo 5. Pemphigus foliaceus in dogs. Crusted erosive dermatitis on the nasal planum with depigmentation and loss of the normal "paving" texture is a unique feature of autoimmune skin disease.

Photo 6. Pemphigus foliaceus in dogs. The same dog from photo 5. Nasal planum lesions are characteristic feature autoimmune skin disease.

Photo 7. Pemphigus foliaceus in dogs.. Crusted papular dermatitis on the auricles of a dog with pemphigus foliaceus. Lesions of the nasal planum, auricles, and pads of the fingers are characteristic features of autoimmune skin disease.

Photo 8. Pemphigus foliaceus in dogs. Alopecia, crusting dermatitis on the margin of the auricle in a Doberman with pemphigus foliaceus. Note the similarity of the lesions to scabies; however, this dog did not have intense itching.

Photo 9 Pemphigus foliaceus in dogs.. Alopecia and crusting papular dermatitis in a Dalmatian. Note the similarity of the lesions to folliculitis.

Photo 10 Pemphigus foliaceus in dogs. Alopecia with crusty papular eruption on the trunk.

Photo 11 Pemphigus foliaceus in dogs. Hyperkeratosis and crusting on the pads of the fingers are characteristic of an autoimmune skin disease. Note that the lesions are on the pad itself more than on the interdigital spaces of the skin. The latter is typical of allergic dermatitis or bacterial or fungal pododermatitis.

Photo 12 Pemphigus foliaceus in dogs. Hyperkeratosis and scabs on the pads of the fingers.

Photo 13 Pemphigus foliaceus in dogs. Hyperkeratosis and crusting on the scrotum of a dog with pemphigus foliaceus.

Photo 14 Pemphigus foliaceus in dogs. Depigmentation of the nasal planum with loss of the normal "cobblestone" texture is an early change associated with autoimmune skin disease.

Photo 15 Pemphigus foliaceus in dogs. Severe moist dermatitis is a rare presentation in pemphigus foliaceus.

Photo 16. Pemphigus foliaceus of cats. Dermatitis of the facial part of the muzzle (alopecia, crusts, papular rash) in a cat. Pay attention to the similarity with dermatitis of the muzzle of Persian cats.

Photo 17. Feline pemphigus foliaceus. Close-up view of the cat in photo 16. Cortical papular dermatitis with alopecia on the muzzle and auricles is a characteristic feature of an autoimmune skin disease.

Photo 18. Feline pemphigus foliaceus. Same cat in photo 16. Crusted, papular rash on the ears is a unique feature of autoimmune skin disease.

Photo 19. Feline pemphigus foliaceus. Same cat in photo 16. Crusted, erosive dermatitis with alopecia around the nipples is a common and unique feature of pemphigus foliaceus in cats.

Photo 21. Hyperkeratosis and scabs on the pads of the fingers are a common feature of autoimmune skin disease.

Photo 22. Feline pemphigus foliaceus. Crusted nail bed dermatitis (paronychia) is a common and unique feature of pemphigus foliaceus in cats.

Photo 23. Feline pemphigus foliaceus. Paronychia and hyperkeratosis of the paw pads in a cat with pemphigus foliaceus.

Photo 24 Pemphigus foliaceus in dogs and cats. Microscopic image of acantholytic cells and numerous neutrophils. Lens magnification 10

Photo 25 Pemphigus foliaceus in dogs and cats. Microscopic image of acantholytic cells. Lens magnification 100

Photo 26. Pemphigus foliaceus in dogs. Pronounced scabs on the pads of the fingers of the affected dog.

Photo 27 Pemphigus foliaceus in dogs. Severe cortical footpad lesions developed within a few weeks in a middle-aged dog.

Photo 28.Severe cortical lesion of the muzzle with alopecia in a cat. nasal mirror affected, but not to the extent that is usually observed in dogs.

Federal Agency for Education

State educational institution

Moscow State University of Applied Biotechnology

Faculty of Veterinary and Sanitary

Course work

in Pathological Animal Physiology

Topic: "Autoimmune diseases of animals"

Moscow - 2006

Abstract………………………………………………………………………….3

Introduction……………………………………………………………….………...3

Literature Review………………………………………………………….....4

1. Tolerance withdrawal and autoimmunity…………………………………...4

2. Autoimmune diseases: general information……………………………..7

3. Etiology and pathogenesis………………………………………………………….8

3.1. Autoimmune diseases: the action of circulating antibodies……..15

3.2. Autoimmune pathology caused by antigens…………………16

3.3. Autoimmune diseases: caused by immune complexes…………17

3.4. Autoimmune pathology caused by organs of immunogenesis…..18

3.5. Cellular immunity: reactions in autoimmune diseases ...... 21

4. Autoantibodies as diagnostic markers……………………………...22

5. Autoimmunity of bulls and reproductive functions………………23

6. Experimental autoimmune diseases…………………………24

7. Antireceptor autoantibodies and their significance in pathology……………..26

8. Autoallergy…………………………………………………………………27

9. Systemic lupus erythematosus…………………………………………………..28

10. Conclusion…………………………………………………………………….32

11. Bibliographic list………………………………………………..33

annotation

This work is devoted to autoimmune diseases in animals. The paper presents several theories about the mechanisms of the occurrence of autoimmune conditions in the animal body. Data from nine sources are given. There are several main theories on this little-studied issue, which are given below.

Introduction

Currently, the issue of autoimmune pathology of animals is one of the first places. Immunology is a relatively young science and the question of the origin and development of autoimmunity is still open.

Autoimmune reactions play important role in the pathogenesis of many animal diseases. The study of autoimmunity has led to the introduction of new methods for diagnosing and treating animal diseases. The study of autoimmune processes is of practical interest.

Knowledge of autoimmunity is very important for a future veterinarian. This pathology is observed more and more often in animals. After all, autoimmunity is the root cause, and the disease will already be a consequence. It is from this point of view that it is necessary to consider diseases caused by autoimmunity.

These diseases are severe and some of them are incurable. They cause damage to agriculture and chagrin to the owners of pets.

Some of the first theories of pathogenesis were only partially correct, but time passes and science does not stand still. Thanks to new research methods, immunologists have many opportunities to study this pathology and theories based on modern knowledge have appeared. The main theories will be presented in this paper below.

Literature review

1. Tolerance withdrawal and autoimmunity

Immunological tolerance is not strictly constant and can be lost, including spontaneously. Spontaneous loss of tolerance occurs due to the removal of the extracellular antigen, the degradation of the intracellular antigen, and the increase in immunocompetent cells as a result of reproduction from hematopoietic stem progenitor cells. Therefore, the rate of loss of tolerance depends on the rate of generation of lymphocytes from stem cells. This process can be accelerated by ionizing radiation of tolerant animals, which accelerates the death of tolerant lymphocytes and replaces them by multiplying hematopoietic stem cells that do not carry a state of tolerance. Conversely, the duration of tolerance can be increased by periodic administration of the antigen.

Cancellation of tolerance in the experiment can be induced by the transfer of normal lymphoid cells, injection of passive antibodies. Loss of tolerance occurs with the introduction of some related antigens (cross-reacting). For example, tolerance to normal serum albumin in mice is abolished when animals are immunized with human serum albumin.

There may be a breakdown of autotolerance and the appearance of an immune response to the antigens of one's own body, i.e., autoaggression, with the development of an autoimmune reaction and autoimmune pathology. Many microorganisms have groups of epitopes that are extremely close in structure, similar to some epitopes of human tissues (antigenic mimicry). Infection with microorganisms that cross-react antigens with human tissue antigens can lead to the abolition of the immune system's tolerance to self-body antigens. For example, cross-reactive antigens are streptococcal membrane antigens and myocardial subsarcolemmal antigens, β-hemolytic streptococcus.

The body's loss of tolerance to its own antigens, that is, the state of the immune system in which antibodies are formed against the antigens of its own body, is called autoimmunity. According to the figurative expression of J. Playfair (1998), autoimmunity is a mirror reflection of tolerance that occurs when regulatory mechanisms for restraining autoreactivity are disrupted, which can lead to autoimmune pathology.

In the body of a healthy animal or person, in the course of normal metabolism, a small amount of autoantibodies against a wide variety of antigenic components of the body are formed to transport these components in the body, mainly for "obsolete" macromolecules that have come out of naturally degrading cellular and subcellular structures. These normal autoantibodies are involved in the regulation of tissue function, favorably affect the growth and differentiation of body cells. In turn, anti-idiotypic antibodies can be formed against idiotypic autoantibodies, resulting in idiot-type-anti-idiotypic interactions. The established balance between idiotypic and anti-idiotypic antibody receptors leads to the emergence of tolerance to its own antigenic determinants (epitopes).

Therefore, normally the immune system coexists with autoimmunity, but is able to control it. At the same time, autoimmune reactions are not a “mistake” of the immune system, but are a key process both for maintaining health and for the formation of autoimmune pathology.

One reason for self-recognition is that the accuracy of antigen-antibody interactions has its limits. Self and foreign antigens consist of the same nucleic acids, proteins, carbohydrates and lipids, and some hormones and enzymes have become almost identical in the course of evolution (at least in terms of their antigenic determinants) in the “own” and “foreign” organisms. In addition, many microorganisms have antigenic determinants of human and animal tissues that are extremely similar in structure.

In connection with the foregoing, it can be assumed that the main causes of the occurrence of autoimmune pathology are the presence of antigenic mimicry in living organisms and violations of the regulatory mechanisms for restraining autoreactivity.

There are various options for the development of an autoimmune response:

the formation of antibodies and cytotoxic T-lymphocytes to their own, unchanged antigens that entered the bloodstream that appeared in the body in the postembryonic period or sequestered (sex cells, antigens of neurons, the lens), which is possible with injuries and inflammatory processes accompanied by a violation of barriers between immunocompetent lymphocytes and the so-called "barrier" antigens;

autoimmune reactions against their cells carrying foreign antigens, such as intracellular viruses (pox virus, Epstein-Barr virus, etc.), a malaria pathogen attached to cells, some drugs (penicillin, etc.), an influenza virus attached to red blood cells. In this case, its own cell, carrying foreign antigens, can be destroyed along with them;

autoantibodies can occur during antigenic mimicry, i.e., in infectious diseases, the causative agents of which have elytols similar to the epitopes of the host's tissue antigens. Such an immune response is possible in the presence of autoreactive B-lymphocytes, when their clonal elimination turned out to be incomplete, as a result of which invasive microorganisms that have antigenic determinants in common with the host cause the production of antibodies both to their own (bacterial) antigens and to host antigens;

dysregulation in the idiotype-anti-idiotypic network due to the loss of suppressor activity in the system of suppressor cells, which can lead to autoimmune pathology;

stimulation of autoreactive B-lymphocytes directly by polyclonal activators (Epstein-Barr virus, malaria pathogens, trypanosomes, graft versus host) bypassing normal activation pathways. In particular, the Epstein-Barr virus directly infects B cells and makes them proliferating for a long time.

SAINT PETERSBURG ACADEMY OF VETERINARY MEDICINE

Department of Pathological Physiology

Abstract on the topic:

Origin mechanisms

Autoimmune pathology can be characterized as an attack of the immune system against the organs and tissues of the body, resulting in their structural and functional damage. The antigens involved in the reaction, usually present in a person or animal and characteristic of them, are called autoantigens, and antibodies capable of reacting with them are called autoantibodies.

Autoimmunization of the body is closely related to the violation of immune tolerance, i.e. the state of unresponsiveness of the immune system in relation to the antigens of its organs and tissues.

The mechanism of autoimmune processes and diseases is similar to the mechanism of immediate and delayed types of allergy and is reduced to the formation of autoantibodies, immune complexes and sensitized T-lymphocytes-killers. Both mechanisms can be combined or one of them predominates.

The essence of autoimmune processes lies in the fact that under the influence of pathogens of infectious and parasitic diseases, chemical substances, drugs, burns, ionizing radiation, feed toxins changes antigenic structure organs and tissues of the body. The resulting autoantigens stimulate the synthesis of autoantibodies in the immune system and the formation of sensitized T-lymphocytes-killers capable of carrying out aggression against altered and normal organs, causing damage to the liver, kidneys, heart, brain, joints and other organs.

Morphological changes in autoimmune diseases are characterized by inflammatory and dystrophic changes in damaged organs. Parenchyma cells show granular dystrophy and necrosis. IN blood vessels mucoid and fibrinoid swelling and necrosis of their walls, thrombosis are noted, lymphocytic-macrophage and plasmacytic infiltrates are formed around the vessels. In the connective tissue of the stroma of the organs, dystrophy in the form of mucoid and fibrinoid swelling, necrosis and sclerosis are detected. in the spleen and lymph nodes expressed hyperplasia, intense infiltration of lymphocytes, macrophages and plasma cells.

Autoimmune reactions play an important role in the pathogenesis of many animal and human diseases. The study of autoimmune processes is of great practical interest. The study of autoimmunity has led to significant advances in the diagnosis and therapy of a number of human and animal diseases.

There is a certain spectrum of manifestations of autoimmune pathology.

Some are characterized by organ damage - organ specificity. An example is Hashimoto's disease (autoimmune thyroiditis), in which specific lesions are observed thyroid gland, including mononuclear infiltration, destruction of follicular cells and the formation of germinal centers, accompanied by the appearance of circulating antibodies to certain components of the thyroid gland.

Generalized or non-organ-specific are characterized by an autoimmune reaction with antigens common to various organs and tissues, in particular, with antigens cell nucleus. An example of such a pathology is systemic lupus erythematosus, in which autoantibodies do not have organ specificity. Pathological changes in these cases affect many organs and are mainly lesions connective tissue with fibrinoid necrosis. The blood cells are also often affected.

At the same time, the autoimmune response to self antigens with the participation of cellular and humoral immunity is primarily aimed at binding, neutralizing and eliminating old, destroyed cells, products of tissue metabolism from the body. Under conditions of a normal physiological state, the degree of possibility of autoimmune processes is strictly controlled.

Diseases associated with tissue damage by autoantibodies may be due to:

1) antigens;

2) antibodies;

3) pathology of the organs of immunogenesis.

Autoimmune pathology caused by antigens

A feature of this pathology is that the tissues of one's own body, either without changes in their antigenic composition, or after its change under the influence of factors external environment perceived by the immunological apparatus as foreign.

When characterizing the tissues of the first group (nervous, lens of the eye, testicles, thyroid gland), two cardinal features should be noted: 1) they are laid later than the immune apparatus, and therefore immunocompetent cells are preserved for them (unlike tissues that are laid before the immune apparatus and secrete factors destroying immunocompetent cells to them); 2) the peculiarities of the blood supply of these organs are such that the products of their degradation do not enter the bloodstream and do not reach the immunocompetent cells. When the hematoparenchymal barriers are damaged (trauma, surgery), these primary antigens enter the bloodstream, stimulate the production of antibodies that, penetrating through the damaged barriers, act on the organ.

For the second group of autoantigens, it is decisive that under the action of external factor(infectious or non-infectious nature), the tissue changes its antigenic composition and actually becomes alien to the body.

Autoimmune pathology caused by antibodies

Has several options:

1. The foreign antigen entering the body has determinants similar to the antigens of the body's own tissues, and therefore the antibodies formed against the foreign antigen "mistake" and begin to damage their own tissues. The foreign antigen may be absent in the future.

2. An alien hapten enters the body, which combines with the protein of the body and antibodies are produced against this complex that can react with each of its individual components, including its own protein, even in the absence of the hapten.

3. The reaction is similar to type 2, only a foreign protein enters the body, reacting with the hapten of the body and antibodies produced against the complex continue to react with the hapten even after the foreign protein is removed from the body.

Autoimmune pathology caused by organs of immunogenesis

The immune apparatus does not contain immunocompetent cells to the tissues of one's own body, which are laid in embryogenesis before the immune system. However, such cells can appear during the life of the organism as a result of mutations. Normally, they are either destroyed or suppressed by suppressor mechanisms.

According to etiopathogenesis, autoimmune pathology is divided into primary and secondary. Autoimmune diseases are primary.

Autoimmune diseases include diabetes, chronic thyroiditis, atrophic gastritis, ulcerative colitis, primary cirrhosis of the liver, orchitis, polyneuritis, rheumatic heart disease, glomerulonephritis, rheumatoid arthritis, dermatomyositis, hemolytic anemia.

The pathogenesis of primary autoimmune pathology in humans and animals is directly related to genetic factors that determine the nature, location, and severity of their accompanying manifestations. The main role in the determination of autoimmune diseases is played by genes encoding the intensity and nature of immune responses to antigens - genes of the major histocompatibility complex and immunoglobulin genes.

Autoimmune diseases may be formed with various types immunological damage, their combination and sequence. The cytotoxic effect of sensitized lymphocytes (primary cirrhosis, ulcerative colitis), mutant immunocytes that perceive normal tissue structures as antigens (hemolytic anemia, systemic lupus erythematosus, rheumatoid arthritis), cytotoxic antibodies (thyroiditis, cytolytic anemia), antigen-antibody immune complexes (nephropathy, autoimmune skin pathology).

Acquired autoimmune pathology is also registered in diseases of a non-infectious nature. An increased immunological reactivity of horses with extensive wounds is known. In cattle, ketosis, chronic feed poisoning, metabolic disorders, beriberi induce autoimmune processes. In young newborns, they can occur by the colostral route, when autoantibodies and sensitized lymphocytes are transmitted through colostrum from sick mothers.

In radiation pathology, a large, even leading role is assigned to autoimmune processes. Due to sharp increase the permeability of biological barriers, tissue cells, pathologically altered proteins and substances associated with them, which become autoantigens, enter the bloodstream.

The production of autoantibodies occurs with any type of irradiation: single and multiple, external and internal, total and local. The rate of their appearance in the blood is much higher than antibodies to foreign antigens, since the body always has the production of normal anti-tissue autoantibodies that play an important role in binding and removing soluble metabolic products and cell death. The production of autoantibodies is even higher with repeated exposure to radiation, that is, it obeys the usual patterns of primary and secondary immune responses.

Autoantigens that can induce autoimmune processes are also formed under the influence of high and low temperatures, a variety of chemicals, as well as some drugs used to treat animals.

Autoimmunity of bulls and reproductive functions

The concentration of the best sires at state breeding enterprises and the use of their semen in artificial insemination has significantly increased the genetic potential of dairy herds. In conditions of widespread use of male sires, the evaluation of the quality of their semen is of great importance.

In cases of autoimmunity to their own semen in males with normal ejaculates in other respects, there is a decrease in the fertilizing ability of the seed and the embryonic survival of their offspring.

Immunological studies of the reproductive ability of breeding males revealed that overheating of the testes causes a violation of spermatogenesis, accompanied by the appearance of autoantibodies in the blood, and that their effect is due to an increase in the permeability of the hematotesticular barrier.

There is also evidence that with age in sires, partial hyaline degeneration of the basement membrane, necrosis, and slippage of the seminal epithelium appear in some convoluted tubules of the testis.

Circulating antibodies to autologous spermatozoa do not always and immediately inhibit spermatogenesis due to the presence of a powerful hematotesticular barrier between blood and seminal epithelial cells. However, trauma, prolonged overheating of the testes and the whole organism, as well as experimental active immunization, weaken this barrier, which leads to the penetration of antibodies into Sertoli cells and spermatogenic epithelium and, as a result, to disruption or complete cessation of spermatogenesis. Most often, the process stops at the stage of round spermatids, but after a long action of antibodies, the division of spermatogonia also stops.

Experimental autoimmune diseases

For a long time, the attention of doctors and biologists has been attracted by the question of whether sensitization against one's own tissue components can be the cause of the disease. Experiments to obtain autosensitization were carried out on animals.

It has been found that intravenous administration of a foreign brain suspension to a rabbit induces the formation of brain-specific antibodies that are able to specifically react with brain suspension, but not other organs. These anti-brain antibodies cross-react with brain suspensions from other animal species, including the rabbit. The animal producing the antibodies showed no pathological changes in its own brain. However, the use of Freund's adjuvant changed the observed picture. Brain suspensions mixed with complete Freund's adjuvant, after intradermal or intramuscular administration, in many cases cause paralysis and death of the animal. Histological examination revealed areas of infiltration in the brain, consisting of lymphocytes, plasma and other cells. Interestingly, intravenous injection of rabbit brain suspension into rabbits (animals of the same species) cannot induce the formation of autoantibodies. However, rabbit brain suspension mixed with Freund's adjuvant causes autosensitization to the same extent as any foreign brain suspension. In other words, brain suspensions under certain conditions can be self-antigens, and the disease caused can be called allergic encephalitis. Some researchers believe that multiple sclerosis may be caused by autosensitization to certain brain antigens.

Another protein has organ-specific properties - thyroglobulin. intravenous injection thyroglobulin obtained from other animal species led to the production of thyroglobulin precipitating antibodies. There is a great similarity in the histological picture of experimental rabbit thyroiditis and chronic thyroiditis in humans.

Circulating organ-specific antibodies are found in many diseases: anti-renal antibodies in kidney diseases, anti-cardiac antibodies in certain heart diseases, and so on.

The following criteria have been established that may be useful when considering diseases caused by autosensitization:

1) direct detection of free circulating or cellular antibodies;

2) detection of the specific antigen against which the antibody is directed;

3) production of antibodies against the same antigen in experimental animals;

4) the appearance of pathological changes in the corresponding tissues in actively sensitized animals;

5) obtaining a disease in normal animals by passive transfer of serum containing antibodies or immunologically competent cells.

A few years ago, when breeding pure lines, a strain of chickens with hereditary hypothyroidism was obtained. Chicks spontaneously develop severe chronic thyroiditis and their serum contains circulating antibodies to thyroglobulin. Searches for a virus have so far been unsuccessful, and it is very possible that there is a spontaneously observed autoimmune disease in animals.

Antireceptor autoantibodies and their significance
in pathology

Autoantibodies to receptors of various hormones are well studied in some types of endocrine pathology, in particular in diabetes, thyrotoxicosis, which allows many researchers to consider them as one of the leading links in the pathogenesis of diseases of the endocrine glands. Along with this, in last years interest in other antireceptor autoantibodies - antibodies to neurotransmitters has also grown, their participation in the regulation of the function of the cholinergic and adrenergic systems of the body has been proven, and their connection with certain types of pathology has been established.

Studies of the nature of atopic diseases, conducted over several decades, have undeniably proved the immunological nature of their launcher- the role of IgE in the mechanism of biological release active substances from mast cells. But only in recent years have more complete data been obtained on the immune nature of disorders in atopic diseases concerning not only the trigger mechanism of allergies, but also the atopic syndrome complex associated with impaired functioning of adrenergic receptors in these diseases, and in particular in asthma. It's about on the establishment of the fact of the existence of autoantibodies to b-receptors in atopic asthma, which puts this disease in the category of autoimmune pathology.

The question of the cause and mechanism of the production of autoantibodies to the b-receptor remains open, although, based on general ideas about the development of allergic diseases, the appearance of autoantibodies can be explained as a consequence of dysfunctions of suppressor cells, or, based on Jerne's theory, by the fact that autoimmunity is the normal physiological state of the immune system and that physiological autoantibodies under the influence of external or internal conditions turn into pathological ones and cause classic autoimmune pathology.

Autoallergy

With various pathological conditions blood and tissue proteins can acquire allergenic properties that are foreign to the body. Autoallergic diseases include allergic encephalitis and allergic collagenases.

Allergic encephalitis occurs when repeated administration of various kinds of extracts obtained from the brain tissue of all adult mammals (excluding rats), as well as from the brain of chickens.

Allergic collagenases represent a peculiar form of infectious autoallergic diseases. The autoantibodies formed in these cases cause a cytotoxic effect in the tissues; there is a lesion of the extracellular part of the connective tissue of a collagenous nature.

Allergic collagenoses include acute articular rheumatism, some forms of glomerulonephritis, etc. Corresponding antibodies were found in acute articular rheumatism. As a result of experimental studies, the allergic nature of acute articular rheumatism was proved.

Many researchers believe that the pathogenesis of rheumatic heart disease is similar to the pathogenesis of rheumatic heart disease. Both of them develop against the background of focal streptococcal infection. In the experiment, when animals were injected with chromic acid, they developed renal autoantibodies and glomerulonephritis. Autoantibodies are nephrotoxins that damage kidney tissue, can be obtained by freezing the kidneys, by ligating the renal vessels, ureters, etc.

autoimmune disease - This is a violation of the activity of the immune system, in which an attack of the organs and tissues of one's own body begins. In other words, the immune system perceives its tissues as foreign elements and begins to damage them.

The immune system is a defense network of white blood cells, antibodies, and other components involved in fighting infection and rejecting foreign proteins. This system distinguishes "self" cells from "foreign" cells by markers located on the surface of each cell. That is why the body rejects transplanted skin flaps, organs and transfused blood. The immune system can malfunction, either due to the inability to do its job, or its overactive performance.

In autoimmune diseases, the immune system loses the ability to recognize "its" markers, so it begins to attack and reject the body's own tissues as foreign.

The mechanism of autoimmune processes is similar to the mechanism of immediate and delayed types of allergy and is reduced to the formation of autoantibodies, immune complexes and sensitized T-lymphocytes-killers.

The essence of autoimmune processes lies in the fact that under the influence of pathogens of infectious and parasitic diseases, chemicals, drugs, burns, ionizing radiation, feed toxins, the antigenic structure of organs and tissues of the body changes. The resulting autoantigens stimulate the synthesis of autoantibodies in the immune system and the formation of sensitized T-lymphocytes-killers capable of carrying out aggression against altered and normal organs, causing damage to the liver, kidneys, heart, brain, joints and other organs.

Autoimmune diseases are organ (encephalomyelitis, thyroiditis, diseases of the digestive system caused by chronic intoxication and metabolic disorders) and systemic (autoimmune diseases of the connective tissue, rheumatoid arthritis). They can be primary and secondary. Primary ones arise as a result of congenital and acquired disorders in the immune system, accompanied by a loss of tolerance of immunocompetent cells to their own antigens and the appearance of prohibited clones of lymphocytes.

A characteristic feature of autoimmune diseases is a long undulating course.

Diagnosis of autoimmune diseases is made on the basis of anamnestic data . Clinical manifestations of the disease, hematological, biochemical and special immunological studies for the detection of antigens, antibodies, antigen + antibody complexes and sensitized lymphocytes.

Autoimmune eye diseases in animals:

• or Chronic superficial vascular keratitis is a lesion of the limbus and cornea of ​​the eye, resulting from local chronic inflammatory process. The infiltrate formed under the corneal epithelium is replaced by scar tissue, which leads to a significant decrease in vision. The immune system considers its own cornea to be a foreign tissue and tries to reject it.

The first reports of pannus appeared in areas with high ultraviolet activity (in Austria and US state Colorado). To date, the disease is registered in all countries of the world. And it's no secret that cases of pannus in areas with increased ultraviolet activity are more difficult and less treatable. This allows us to conclude that ultraviolet rays play an important role in the occurrence of this disease. This phenomenon is due to the fact that exposure to ultraviolet radiation on the cornea accelerates the rate of metabolic processes in the latter. And the more active metabolic processes, the more actively the immune system tries to reject it.

This pathology is most common in dogs of breeds such as German Shepherd, Black Terrier and Giant Schnauzer. It is much less common in dogs of other breeds.

• or Plasma lymphatic conjunctivitis of the third eyelid is a state in which a similar immune response affects the conjunctiva and the third eyelid. Plasmoma is less threatening to loss of vision, but delivers more ocular discomfort.

MINISTRY OF EDUCATION AND SCIENCE

REPUBLIC OF KAZAKHSTAN

KAZAKH NATIONAL AGRARIAN UNIVERSITY

Faculty of Veterinary Medicine and Biotechnology

Department of Obstetrics and Surgery

GRADUATE WORK

on the topic: Autoimmune skin diseases in dogs

Performed

Group 406 student

Silchenkova Natalya

Head Muralinov K.K.

Almaty 2010

Introduction

Autoimmune diseases are a large group of diseases that can be combined on the basis that the immune system that is aggressively tuned against its own body takes part in their development.

The causes of almost all autoimmune diseases are still unknown. Given the huge variety of autoimmune diseases, as well as their manifestations and the nature of the course, these diseases are studied and treated by a variety of specialists. Which one depends on the symptoms of the disease. So, for example, if only the skin suffers (pemphigoid, psoriasis), a dermatologist is needed, if the lungs (fibrosing alveolitis, sarcoidosis) - a pulmonologist, joints (rheumatoid arthritis, ankylosing spondylitis) - a rheumatologist, etc.

However, there are systemic autoimmune diseases when various organs and tissues, eg, systemic vasculitis, scleroderma, systemic lupus erythematosus, etc. (or the disease "goes" beyond the scope of one organ, for example, when rheumatoid arthritis not only the joints can be affected, but also the skin, kidneys, lungs), in such situations, most often the disease is treated by a doctor whose specialization is associated with the most striking manifestations of the disease or several different specialists.

The prognosis of the disease depends on many reasons and varies greatly depending on the type of disease, its course and the adequacy of the therapy.

The treatment of autoimmune diseases is aimed at suppressing the aggressiveness of the immune system, which no longer distinguishes between "self and others." Medicines, aimed at reducing the activity of immune inflammation, are called immunosuppressants.

The main immunosuppressants are prednisolone (or its analogues), cytostatics (cyclophosphamide, methotrexate, azathioprine, etc.) and monoclonal antibodies, which act as specifically as possible on individual links of inflammation.

Suppress immune system with autoimmune diseases it is not possible, but necessary, not for everyone, of course, and the intensity of treatment will depend on the type of disease. The doctor always weighs on the scales what is more dangerous: the disease or the treatment, and only then accepts the treatment. So, for example, with autoimmune thyroiditis, it is not necessary to suppress the immune system, but with systemic vasculitis (for example, microscopic polyangiitis) it is simply vital! You can live with suppressed immunity for many years, but the frequency is increasing infectious diseases, this is a kind of "fee" for the treatment of the disease. Autoimmune diseases are often difficult to diagnose and require special attention doctors, very different in their manifestations and prognosis.

The purpose and objectives of the research:

To give a theoretical justification for the use of the immunomodulator anandine and methyluracil ointment for the treatment of autoimmune skin diseases.

In accordance with the set goal, the specific objectives of our research were:

To study the effect of the immunomodulator anandin and methyluracil ointment on clinical and morphological parameters in animals with autoimmune diseases skin;

To study the effect of the immunomodulator anandine and methyluracil ointment on some biochemical indicators of autoimmune skin diseases.

To study the effect of anandine immunomodulator and methyluracil ointment on cellular and humoral factors of nonspecific resistance, as well as immune reactivity of the organism of autoimmune skin diseases.

To study the effect of anandine immunomodulator and methyluracil ointment on regenerative processes in autoimmune dermatitis.

1. LITERATURE REVIEW

1.1 Autoimmune skin diseases

Most known diseases are:

Pemphingoid.

·Psoriasis.

· Discoid lupus erythematosus.

· Isolated skin vasculitis.

· Chronic urticaria(urticarial vasculitis).

· Some forms of alopecia.

Vitiligo.

In general, all skin diseases can be divided into several broad groups: Pyoderma is a pustular disease caused by pyogenic microorganisms (staphylococcus, streptococcus, etc.). Pyoderma is the most common autoimmune dermatitis skin disease in any age groups. These include folliculitis, sycosis vulgaris, furunculosis<#"justify">1.2 Pathological changes in the skin

At the heart of any skin diseases lie a variety of pathomorphological processes occurring in different layers of the skin (epidermis, dermis, hypodermis). The totality of these changes is specific for each disease and is taken into account in its diagnosis, and is often the basis for making a diagnosis. There are two groups of pathological processes according to their localization: in the epidermis and in the dermis. Pathological processes in the epidermis are associated with a change in epidermal kinetics - these are hyperkeratosis, gaustoimmune dermatitis, acanthosis; violation of the differentiation of epidermal cells - parakeratosis, dyskeratosis; violation of epidermal connections - acantholysis, ballooning and vacuolar dystrophy, spongiosis. Pathological processes in the dermis: papillomatosis, microcirculation disorders in the skin, connective tissue degeneration, edema, etc.

1. Hyperkeratosis is a thickening of the stratum corneum of the epidermis, which occurs due to an excess content of keratin. seen in red lichen planus <#"justify">The clinical picture of the allergic form of the disease is as follows: the skin area turns red without the formation of clear gaustoimmune dermatitis and swells; microvesicles, hemispherical vesicles with transparent or cloudy contents are formed on it, which, when opened, leave behind weeping microerosions, scales, and crusts.

The clinical picture of allergic dermatitis differs from the simple one in that the first one affects the skin not only at the site of exposure to the irritant, but also the autoimmune dermatitis spreads beyond its impact. So, for example, the consequences of an allergic reaction to low-quality mascara can spread autoimmune dermatitis on the skin of the face, neck and even chest. The subjective sensations of the patient are most often characterized by severe itching.

The treatment of simple form dermatitis is usually directed at the inflammatory irritant dermatitis, and is based on the application of local funds(lotions with a solution of boric acid, lead water, corticosteroid ointments, epithelizing ointments, disinfectant ointments). At chemical burn The first necessary measure to be taken should be to flush the skin with plenty of water. In the case of a severe form, dermatitis is treated in a hospital.

Diagnosis of autoimmune dermatitis is usually carried out on the basis of anamnesis (the presence of cases of skin exposure to irritants of a chemical or physical nature) and the clinical picture. Sometimes as additional diagnostics various skin tests with the suspected allergen; they are carried out only after the elimination of clinical changes in the skin. Differential Diagnosis is to distinguish between allergic dermatitis and acute stage eczema<#"justify">Clinical picture of lupus erythematosus. There are three stages in the course of discoid lupus erythematosus. The first stage is erythematous; a small, slightly edematous patch of pale pink color appears on the skin. As a rule, it has a clear gaustoimmune dermatitis and gradually increases in size.

The second stage - hyperkeratotic-infiltrative - is characterized by infiltration of the spot, the appearance on its surface of small grayish-white scales, which are difficult to detach and very painful (Besnier-Meshchersky symptom), and small spikes plunging into the mouths of the follicles. The lesion from a pale pink spot gradually turns into a disc-like plaque that is dense to the touch. In the third stage of the disease (atrophic), in the center of the disc-shaped lesion, a smooth, tender, alabaster-white cicatricial atrophy is formed, which gradually spreads over the entire surface of the lesion as a result of autoimmune dermatitis.

The disease is characterized by a long continuous course with periodic relapses, observed mainly in the spring-summer period, which is explained by increased photosensitivity.

With frequent and prolonged exposure to factors that provoke the development and recurrence of discoid lupus erythematosus, the disease can turn into system form.

Biett's centrifugal erythema is a superficial variant skin form lupus erythematosus. It is characterized by pronounced hyperemia, but the absence of scales and cicatricial atrophy, as in discoid lupus erythematosus.

The disease is localized on the skin of the face, usually on the cheeks, and resembles a butterfly in shape. Like discoid lupus erythematosus, Biett's centrifugal erythema is often the initial stage of systemic lupus erythematosus.

Chronic disseminated lupus erythematosus is a multiple focal skin lesion of the discoid type or Biett centrifugal erythema type, which can be located anywhere on the skin of the body.

Deep lupus erythematosus of Kaposi-Irgang is characterized by all the above symptoms of the disease. In addition, in the subcutaneous tissue, one or more dense to the touch, sharply otgatoimmune dermatitis mobile elements are found - lupus panniculitis. After disappearing, they leave behind ugly rough scars. The difference between this form of the disease and the previous ones is that it never forms tautoimmune dermatitis into systemic lupus erythematosus.

Lupus erythematosus (lupus erythematodes), syn. erythematosis is a skin disease of a group of diffuse connective tissue diseases.

There are two forms of the disease: cutaneous (integumentary), characterized by damage to the skin only, and systemic lupus erythematosus.<#"justify">· disorders of a neuroendocrine nature: dysfunction of the thyroid gland, adrenal glands, pituitary gland, gonads;

· mental trauma;

· disorders of the autonomic nervous system (the predominance of the tone of the sympathetic part of the autonomic nervous system over the tone of its parasympathetic part);

· autoimmune processes;

· hereditary predisposition, which is confirmed by family cases of the disease.

Violation of skin pigmentation is presumably due to blocking of the tyrosinase enzyme, an enzyme involved in the biosynthesis of melanin pigments. In addition, some cases of this disease are classified as Occupational Illness caused by exposure to alkylphenols (tert-butylphenol, butylpyroxatechin), polyacrylates.

Histologically, in the newly appeared spots and foci of vitiligo, a small number of melanocytes with signs of degeneration are found, in long-term foci - complete absence melanocytes. In the dermis, there is a slight expansion of blood vessels, accumulations of fibroblasts, histiocytes, basophils; hair follicles, sebaceous and sweat glands are moderately atrophied.

On the skin there are depigmented spots of various sizes, outlines and shapes, prone to peripheral growth. The spots are surrounded by a zone of moderate hyperpigmentation, which gradually turns into normally colored skin. Very rarely, in patients, the spots are bordered by a narrow corolla that rises slightly above the level of the skin. Growing, the spots tend to merge with each other, forming extensive foci. In the foci, the hair changes color, turns pale; sweating and sebum secretion, vasomotor and muscular-hairy reflexes are disturbed.

Vitiliginous spots and foci can be localized on any part of the skin: on the back of the hands, in the area of ​​the wrists, forearms, face, neck, genitals; more often they are arranged symmetrically. There are cases of damage to almost the entire skin, unilateral lesions.

Often vitiligo is accompanied solar dermatitis.

The diagnosis of vitiligo is made on the basis of the clinical picture and in most cases does not cause difficulties, due to the characteristic clinical manifestations diseases. Differential Diagnosis carried out with pityriasis versicolor<#"justify">· first of all, it is aimed at the factor that provoked the development of the disease: ustautoimmune dermatitis neurotic disorders, elimination of neuroendocrine disorders, exacerbations of chronic diseases, hypoallergic diet;

· hyposensitizing therapy (solutions of sodium thiosulfate, calcium chloride intravenously, calcium gluconate, magnesium sulfate intramuscularly);

· antihistamines (diphenhydramine, pipolfen, suprastin, tavegil, diazolin, cimetidine, duovel, zaditen, peritol);

· at severe forms eczema are prescribed corticosteroid hormones (prednisolone);

· immunocorrective agents (decaris, taktivin, thymalin, diucifon, methyluracil, pentoxyl);

· at acute form prescribe hemodez, diuretics;

· at microbial eczema vitamins of group B, purified sulfur are shown, with dyshidrotic - bellataminal;

· external treatment: lotions with boric acid, silver nitrate, dimexide (with acute weeping eczema); diprosalic solution, sulfuric ointment, salicylic ointment, boric ointment, cream with ketoconazole, triderm ointment (for seborrheic eczema); dermozolon, celestoderm, lorinden C, diprogent, Wilkinson's ointment, Castellani liquid (for microbial eczema); baths with potassium permanganate, followed by opening and quenching of the bubbles (with dyshidrotic eczema).

In the treatment of eczema, physiotherapeutic procedures are widely used: electrophoresis, UV irradiation, UHF therapy, paraffin therapy, mud therapy, acupuncture, etc.

Prevention of the disease consists in: 1. Compliance with the rules of personal hygiene. 2. Timely detection and treatment of other skin diseases (pyoderma, mycosis of the feet<#"justify">Clinical picture of scleroderma. Plaque scleroderma is the most common form of oautoimmune dermatitis scleroderma. It is characterized by the appearance of one or more lesions, localized mainly on the trunk and limbs. The lesions range in size from 1 cm to 15 cm and can be of various shapes (oval, round or irregular). There are three stages of formation and development of the focus: the stage of erythema, the stage of compaction and the stage of atrophy.

initial stage characterized by the appearance of mildly inflammatory erythema of a bluish-pink color. After some time, a seal is found in the center of the focus, the color of which can vary from white to ivory. A thin lilac rim is visible along the edges of the seal. Sometimes blisters appear on the surface of some lesions, some of which are filled with hemorrhagic contents. The stage of atrophy is the stage of regression of the focus, after which hyperpigmentation remains.

Linear scleroderma .The type of lesion and the nature of the severity depend on the location of the foci: foci located on the limbs cause atrophy of deep tissues, including muscle and bone; on the scalp, lesions often move to the skin of the forehead and nose, affect the skin and underlying tissues; on the penis, the focus has the form of a ring in the head groove.

Some doctors distinguish white spot disease as a variant of oautoimmune dermatitis scleroderma, but this point of view is not generally accepted. Small whitish lesions appear on the skin with thin atrophied skin and an erythematous corolla along the edges. Subsequently, small foci merge, forming large foci up to 10 cm in size or more.

With Pasini-Pierini atrophoderma, lesions are localized mainly on the trunk. They have a pink-blue color, gradually turning into brown; compaction may be mild or absent altogether. This form of the disease is often accompanied by plaque or linear scleroderma.

In systemic scleroderma, the entire skin is affected. The skin swells, acquires a waxy white color, becomes dense to the touch and inactive. In the process of development of the disease, three stages are also distinguished: edema, sclerosis and atrophy. The first stage is characterized by the appearance of edema, more pronounced on the trunk, which subsequently spreads to other parts of the body as an autoimmune dermatitis. Skin on the body, in large skin folds, in the genital area is compacted; compacted in the area of ​​​​the joints, it interferes with the movement of the fingers. Facial expressions are difficult, it resembles a mask. In connection with the narrowing of the esophagus, the patient has difficulty swallowing food. Last stage Systemic scleroderma is characterized by atrophy of the skin and muscles, which leads to poikiloderma, hair loss.

Treatment for scleroderma depends on the type of disease. With systemic scleroderma, the patient is prescribed antibiotics (penicillin), lidase injections, antihistamines, antiserotonin drugs (diazolin, peritol). Showing drugs that improve microcirculation and tissue metabolism (teonikol, reserpine, pentoxifylline, cinnarizine). After the main course of treatment for scleroderma, injections of andecalin, vitamins A, E, biogenic preparations(aloe, vitreous body). In severe cases or with severe immune disorders apply plasmapheresis, hemosorption, corticosteroid drugs in small doses. From physiotherapeutic procedures warm baths, paraffin, mud are shown.

With oautoimmune dermatitis scleroderma, penicillin and lidase are also prescribed. Local lesions are lubricated with corticosteroid ointments.

In linear scleroderma, phenytoin is prescribed, antimalarial drugs. Dimexide is applied locally. Phonophoresis, Bernard's diadynamic currents, vacuum therapy, helium-neon or infrared laser beams, paraffin, mud are recommended.

The prognosis depends on the stage and form of the disease: with an autoimmune dermatitis form, the prognosis is good in most cases, with systemic scleroderma, especially with multiple lesion internal organs, the prognosis is less favorable, possible death.

allergic dermatitis pathological focus

2. Own research

2.1 Material and research methods

The work was carried out from 2007 to 2010. at the Department of Obstetrics and Surgery and the Kazakh National Agrarian University with sick animals in the farms of the Almaty region.

The experiment involved 26 dogs of different sex and age groups with autoimmune skin lesions. Animals had previously been repeatedly treated, but recovery did not occur. The animals in the experimental group received anandine and methyluracil ointment. In the control group of animals, treatment was carried out with fluorocort ointment and the immunomodulator catazal was used.

The diagnosis of the disease was combined with anatomical data, pathoanatomical and pathophysiological changes characterizing the staging of the disease, the severity of the process, and the features of the body's response to the stimulus.

The phagocytic activity of leukocytes was determined by the method of Berman and Slavskaya (1958), the degree of phagocytosis was the indicator of the phagocytic number - the percentage of active leukocytes that captured microbes. The phagocytic number gives an idea of ​​the absorptive capacity of leukocytes (phagocytes). A decrease in the phagocytic number to 50 is considered significant, and to 35-40 - sharp. Reducing the phagocytic index to 2.5-3 and the index of phagocytosis completion to 45-50% is an unfavorable indicator.

The number of erythrocytes and leukocytes was counted in the Goryaev chamber, the erythrocyte sedimentation rate was determined by the Panchenko apparatus, the hemoglobin content was determined by the Saly hemometer, the alkaline reserve of blood according to Kondrakhin, the content total protein according to Lowry and Kushmanov, the amount of immunoglobulins according to McEvans and Kostin.

Statistical processing of the obtained results was carried out by the constant method of mathematical analysis of quantitative indicators according to Sazovsky. The level of significance was determined using the Student-Fisher test.

2 Analysis and discussion of research results

In the experiment, 26 dogs of age and sex groups with long-term non-healing autoimmune skin diseases were used, which were divided into 2 groups of 19 animals each. 7 injections and externally methyluracil ointment. In the control group of animals, treatment was carried out with fluorocort ointment and the immunomodulator catazal was used.

The results of studies of the dynamics of the clinical and morphological status of animals during treatment are shown in tables 1 and 2. In all experimental animals, starting from the first day, after the start of treatment, autoimmune dermatitis was observed

The results of the study of the dynamics of the clinical and morphological picture in animals during the treatment of autoimmune dermatitis are shown in Table 1.

In all experimental animals, starting from the first day after the start of treatment, it was observed fever body. The greatest rise in temperature in control animals was observed on the 3rd and 7th days, compared with the experimental ones, they were higher by 0.50 C - 1.50 C. Then, starting from the 14th to the 21st day of observation, the greatest rise in temperature was noted body from 2.20 C to 1.90 C. Then the temperature in the experimental animals slowly decreased from 1.50 C to 0.60 C and only on the 21st day were within normal physiological parameters.

In all experimental animals, the pulse increased by an average of 8.9% from the first to the 5th day. The greatest increase in heart rate was observed on the 7th and 14th days by an average of 26.2 - 28.7%.

Table 1 - Dynamics clinical indicators in animals in the experimental group

No. p / n Time of study (days) Temperature (0С) Pulse rate (bpm) Respiratory rate (d.d. min) 11 days 40.50 ± 0.16 xxx74.40 ± 1.07 xxx33.40 ± 1.09 ххх2On the 3rd day39.45 ± 0.15 хх70.00 ± 0,8928,80± 0.64 ххх3On the 7th day39.27 ± 0,1270,60± 1,2927,10± 0.69 хх4On day 1439.19 ± 0,0869,70± 1,0425,80± 0.645On day 2138.98 ± 0,0768,60± 1,1824,80± 0.956On day 2838.94 ± 0,0868,20± 1,1723,90± 0.94x; - R<0.05 x - относительно здоровых животных хх; - Р<0.01 ххх- Р<0.001

Table 2 - Dynamics of clinical indicators in control animals

No. p / p Terms of study (days) Temperature ( º C) Pulse (beats/min) Respirations (d.d/min) 1.1 days 38.72 ± 0,1565,80± 1,1923,60± 0.742On day 339.09 ± 0,1869,00± 1,1424,00± 0.543s 7 days39.20 ± 0.08хх67.60 ± 1,5326,40± 0.65хх4On the 14th day39.80 ± 0.07ххх70.60 ± 1.34хх29.00 ± 0.75ххх5On day 2140.71 ± 0.18ххх74.80 ± 1.26ххх32.10 ± 1.15ххх6On day 2840.65 ± 0.14ххх76.60 ± 1.00ххх31.70± 0.82xxx

On the 21st day, the pulse rate gradually decreased, but in the control group it practically did not stabilize during the end of the observation to the values ​​of the experimental animals.

In control animals, after the start of treatment of the disease, the number of respiratory movements increased, starting from the first day of observation until the 3rd day, by an average of 26.7% than in animals in the experimental group. On days 7 and 14, the number of respiratory movements increased from 37.2% to 43.6%. Then, starting from the 21st day, the number of respiratory movements gradually decreased and on the 28th day it reached the level of the initial parameters. In animals, on average, the number of respiratory movements fluctuated within 19.1%, the reliability coefficient was high.

In the experimental group, it was noted in individual animals starting from the 14th day. The fluctuation of healing in comparisons of the area of ​​autoimmune dermatitis in animals in the experimental and control groups averaged 12-14%.

The results of morphological and biochemical studies of peripheral blood in animals in the experimental and control groups are shown in Tables 3 and 4. day - by 16.2%, on the 21st day - by 14.9%, compared with the initial indicators. On the 28th day, the number of erythrocytes reached the limits of indicators to a traumatic state

The amount of hemoglobin in animals in the control group compared with the experimental group on the 3rd day from the start of treatment decreased by 5.1%, on the 7th day in the experimental group compared to the control group increased by 3.6%, on the 14th day the increase was 14.7% on the 21st day - 5.6% and at the end of the observation period on the 28th day was within the limits of a healthy state.

Table 3 - Dynamics of morphological blood parameters in experimental animals

No. p/p Time of study (days) The number of red blood cells (10 12) The amount of hemoglobin (g/l) The total number of leukocytes (х10 9) The total protein (g/l) 1.1 day 5.18 ± 0,1893,60± 2,48**8,81± 0,37***5,48± 0.22***2. On day 35.12 ± 0,1585,20± 1,7113,86± 0,476,32± 0.153. On the 7th day 6.67 ± 0,25***89,44± 2,2913,53± 0,446,11± 0.144. On the 14th day 6.24 ± 0,21***91,97± 1,12***11,95± 0,22***6,25± 0.135. On the 21st day 6.15 ± 0,18***92,75± 1,29***10,65± 0,27***6,44± 0.116. On the 28th day 6.13 ± 0,14***93,77± 1,16***9,56± 0,33***6,58± 0.14x; * - R<0.05 x - относительно здоровых животных хх; **- Р<0.01 * - относительно больных животных ххх; *** - Р<0.001

Table 4. Dynamics of hematological parameters in the blood in the control group of animals

No. n / n Time of study (days) Number of erythrocytes (10 12) Amount of hemoglobin g / l Total number of leukocytes 109 Total protein g / l 11 days 7.30 ± 0,1082,20± 3,178,35± 0,245,46± 0.272On day 37.70 ± 0.14x91.90 ± 3.16x9.37 ± 0.32x5.25 ± 0.213On the 7th day7.56 ± 0,1984,20± 3,239,92± 0.33ххх5.46 ± 0.214On day 147.32 ± 0,1580,00± 2,7410,51± 0.34ххх6.34 ± 0.465On day 217.16 ± 0,1584,60± 2,0613,09± 0.55ххх6.53 ± 0.306On day 287.49 ± 0,1188,60± 2.82хх13.12 ± 0.37ххх5.79± 0,34

The total number of leukocytes in the experimental animals increased by 12.6% after 3 days, by 14.3% on the 7th day, and by 38.7% on the 14th day.

An increase in leukocytes was observed up to 21 days up to 61.5%. Then, subsequently, the total number of leukocytes gradually decreased and on the 28th day was within the approximate range of normal values.

The total blood serum protein in experimental animals in comparison with the control animals slightly decreases at the beginning of treatment, and then, starting from the 7th day, it increases by 14.9%, on the 14th day - by 19.3%, on the 21st day - by 8, 4 %. Starting from the 21st day, the level of total blood protein gradually decreased and on the 28th day was within the initial values.

An inverse correlation was established between the amount of hemoglobin and the total number of leukocytes (r=0.78). The results of studying the dynamics of the clinical and morphological status of animals in the treatment of infected with autoimmune dermatitis, it was found that starting from the injury in animals, there is a violation of the homeostasis of the body, both local and general. With treatment, the disease takes a favorable course. In sick animals, the clinical and morphological status, general condition are normalized, appetite appears, and the vitality of the body increases.

2.3 Immunological status of animals during the treatment of infected autoimmune dermatitis

The conducted studies (Tables 5 and 6) showed that in animals in all groups after the start of treatment for the disease, the content of lysozyme on the 3rd day after injury in control animals decreased by 14.6% compared with the experimental group, and then began to increase by 14.6%. The 7th day from the development of the disease reached the initial indicators as in healthy animals. On the 14th day of observation, the content of lysozyme increased by 12.6%, on the 21st day - by 9.2%, and on the 28th day it was within the initial values.

Table 5. Dynamics of humoral factors after immunocorrective treatment in the experimental group

No. p/n Study time (days) Lysozyme content U/ml. .4314.90±0.162.18+0.060.54±0.023 On the 7th day 7.24±0.3515.21±0.182.35±0.050.50±0.034 On the 14th day 7.43±0.3915.43±0.182.31 ±0.040.50+0.035 On day 217.82+0.3714.98±0.222.29+0.060.51+0.026 On day 287.60+0.3614.61±0.092.30±0.050.51±0.01x ; * - R< 0.05 х - относительно здоровых животных хх; **- Р<0.01 * - относительно больных животных ххх; *** - Р< 0.001

Table 6. Dynamics of humoral immunity in animals in the control group

No. p/pDuration of the study (days) The content of lysozyme units / ml. Ig J % Ig M % Ig A % 11 days 7.74 ± 0,3814,15± 0,191,91± 0,040,44± 0.022On day 37.70 ± 0,3514,35± 0,151,93± 0,030,56± 0.02ххх3On the 7th day7.07 ± 0,2914,58± 0,152,16± 0.07хх0.63 ± 0.04ххх4On day 146.84 ± 0,2914,77± 0.18x2.41 ± 0.06ххх0.66 ± 0.03ххх5On day 217.46 ± 0,3015,04± 0.18хх2.20 ± 0.07ххх0.61 ± 0.03ххх6On day 287.25 ± 0,2815,22± 0.13ххх2.14 ± 0.06хх0.54± 0.03x

The amount of Ig G in control animals from the first hours after injury increased by 5.3% on the 3rd day. On the 14th day after the onset of the pathology, the increase in the content of immunoglobulin J was 8.5%, on the 21st day - 6.2%. On the next day from the beginning of the experiment, the content of immunoglobulins G gradually decreased and on the 28th day it returned to normal within natural limits.

The amount of immunoglobulins M in control animals, compared with experimental ones, increased on the 3rd day by an average of 6.7%. On the 7th day after the development of the picture of autoimmune dermatitis of the process, the increase was 86.2%. On the 14th day, the content of immunoglobulins M increased by an average of 35.3%. Subsequently, the content of immunoglobulins M slightly decreased and on the 28th day the increase was 36.2%.

The content of immunoglobulins A in animals in the control group after the start of treatment compared with the experimental group increased by 3 days by 42.3%, by 7 days - by 36.4%, and on the 14th day the increase was 22.6%. Then, throughout the entire observation period, there was a gradual decrease in the amount of immunoglobulins A, and on the 28th day after the end of the observation, the increase in the content was within 21.4%.

The results of the study of blood sera of animals with infected autoimmune dermatitis were used to study the genesis of such immunological parameters as bactericidal activity of blood, the amount of immunoglobulins and the content of lysozyme. It has been established that during the immunocorrective treatment process, the largest pronounced fluctuations in immunological parameters in experimental animals occur on the 7th day from the start of treatment for autoimmune dermatitis pathology and last up to 21 days.

A complete correlation between immunological parameters and the clinical state of the body was revealed. A direct correlation was established on the amount of the ratio between Ig M (r=0.38) and the content of lysozyme (r=-0.07).

The study of the dynamics of the immune response indicators showed that during immunocorrective treatment in animals on the 7th and 14th days there is an increase in the bactericidal activity of blood serum, the content of immunoglobulins J, M, A, as well as the content of lysozyme.

Studies have shown that in the course of autoimmune dermatitis without stimulation of therapeutic intervention, the course of reparative processes in sick animals is poorly regulated by the body's immune factors. The initial reparative processes occur starting from the 7th day, the complete restoration of the immunological status in animals with acute surgical injuries is completed on the 19th - 26th day from the start of the treatment of the disease. The data obtained indicate a correlation between the immunobiological status and the regulatory function of the body's homeostasis.

4 Analysis and discussion of research results

In the treatment of autoimmune dermatitis and autoimmune skin diseases, drug intervention should primarily involve the impact on the damaging agent, on various parts of the nervous system, which is a natural regulator of all processes in the body and on the immune system that provides homeostasis of the body.

The priority of active stimulating treatment of the disease does not exclude the traditional method of local drug treatment, which is cost-effective, applicable in any conditions and, therefore, attracts with its accessibility and simplicity.

The existing system of drug treatment of autoimmune dermatitis also has obvious drawbacks. The main one is that the drugs used have a relatively weak therapeutic effect, in most cases insufficient to suppress the autoimmune process and stop the inflammatory process.

Some of the drugs used for long-term use inhibit cell growth, proliferation processes, phagocytic and immunobiological reactions, that is, those processes on which the body's fight against the harmful effects of the external environment depends. Cause symptoms of intoxication and symptoms of unresponsiveness. The effect of various drugs on the body's immunological resistance in traumatic injuries remains insufficiently studied.

In medical and veterinary practice, various drugs are used that are aimed at stimulating reparative processes in dermatitis. However, all drugs used today for these purposes do not give the proper, desired result, and therefore, the search continues for more effective, easily accessible and at the same time inexpensive and requiring less complex manufacturing technologies.

The existing system of drug treatment of autoimmune dermatitis is that the drugs used have a relatively weak therapeutic effect, in most cases insufficient to stop the inflammatory process, do not provide the desired rapid suppression of allergization.

Great changes in practical medicine and surgery have been brought about by the discovery and widespread use of a huge number of the latest generation of immunomodulators, and in veterinary practice these drugs have not yet found wide application, skillful use without knowledge of the mechanism of action, the course of application, worked out on each type of animal, they can have and negative effect on the body.

Therefore, it is extremely necessary in veterinary medicine to test such immunostimulating agents and preparations that would have a completely tangible ability to change the course of inflammatory regenerative processes.

Factors of immunobiological resistance are the most informative in terms of assessing the state of homeostasis. With their help, it is possible to get an idea of ​​the level of resistance of the organism in relation to various adverse environmental influences.

To determine the natural resistance in the blood serum of experimental animals, changes in the number of erythrocytes, hemoglobin, leukocytes and total protein, as well as such clinical indicators as temperature, pulse rate and respiration, as well as the repair of the inflicted disease in dynamics after treatment until complete healing were studied.

Studies have confirmed the complete relationship between the general resistance of the organism and the course of autoimmune dermatitis, which largely determines the timing of recovery.

Therefore, the study of immunobiological signs, traumatic injuries, will determine the prognosis for the development of autoimmune dermatitis. The system of research proposed by us makes it possible to predict the nature of healing in patients with traditional methods of treating autoimmune dermatitis with a high probability.

Conducted studies have found that the course of repair in case of autoimmune dermatitis damage without any medical procedure in sick animals is determined by the state of the activity of the immune system of the organism itself. Proliferative processes in damaged tissues prevail in the second phase of the biology of autoimmune dermatitis of genesis, according to our observation, starting from the 7th day after receiving an acute injury. A full recovery of immunological parameters in sick animals occurred approximately on the 19th - 26th day from the infliction of the disease. Almost complete repair of the damaged surface of the disease also occurred at this time. Therefore, in order to stimulate reparative processes and increase the body's resistance, it is necessary, in addition to the generally accepted methods of medical care, to include immunocorrective therapies.

2.5 Characteristics of the veterinary clinic Mastino

The experiments were carried out in the Mastino veterinary clinic, which occupies an area of ​​65 m2 and is located in 4 rooms: one of them is a pharmacy, the second one receives sick animals, and the third room provides medical assistance to surgical and non-contagious patients. The clinic has a hospital for the treatment of sick animals, it also has an equipped operating room for conducting and demonstrating surgical treatment to students of the veterinary faculty.

The Mastino clinic is equipped with the most modern all necessary devices, equipment and tools. There is an ultrasound room, a laboratory for biochemical and immunological studies.

There are 6 qualified veterinarians with extensive experience and work experience in the staff of the clinic.

Reception of animals is carried out by a therapist, a surgeon and an infectious disease specialist. The clinic is open around the clock. Senior students are assigned to duty together with veterinary specialists. When receiving and treating sick animals, they help and assist the veterinarian.

2.6 Cost effectiveness of veterinary interventions

Cost-effectiveness was determined with various treatments.

The damage prevented as a result of the treatment of sick animals (PU2) was determined as the difference between the possible economic damage from the case, forced slaughter of animals and the loss of production, the actual damage caused by the disease as a result of illness and death of animals according to the formulas:

PU2 \u003d Mz x Cl x Ku2 + Mp x Kuz - U

where: DP2 --- damage prevented as a result of treatment of sick animals

Cl - animal mortality rate

Ku2 - coefficient of damage per one dead animal

Mn - the number of recovered animals

Kuz is the coefficient of damage per ill animal

Y - actual economic damage.

PU2 = 26 x 0.2 x 45,000 + 26 x45,000 - 45,000 = 112,523 tenge

With autoimmune dermatitis in sick dogs, pronounced clinical, morphological and biochemical changes occur in the peripheral blood. A decrease in the content of total protein, erythrocytes, hemoglobin and lysozyme, an increase in leukocytes was established.

For the treatment of patients with autoimmune dermatitis, the use of anandine and levamicol ointment has an effective therapeutic effect.

The use of anandine significantly accelerates the regeneration of the skin and the restoration of morphological and biochemical parameters of blood in animals with allergic dermatitis.

The use of anandine does not cause a recurrence of autoimmune dermatitis, unlike hormonal drugs.

Practical Suggestions

When diagnosing autoimmune dermatitis in patients, it is necessary to determine the forms of the course and eliminate the etiological factors that caused its occurrence.

For the treatment of autoimmune dermatitis in dogs, it is recommended to use the immunomodulator anandine and levamicol ointment.

List of used literary sources

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