Autoimmune skin diseases in cats. Autoimmune skin diseases in dogs. Pemphigus foliaceus and erythematous

Diseases in this group are the result of an inability immune system distinguish “one’s own” from “another’s”. As a result, the body produces autoantibodies, that is, antibodies against the tissues of its own body. Some of these diseases are known as “immune-mediated” and develop due to the formation of antigen-antibody complexes. Autoimmune diseases can be triggered by bacteria, viruses, drugs, tumors and possibly vaccinations.

YOGA is the most common of all immune system diseases in dogs. In this disease, the immune system attacks and destroys the body's own red blood cells. This reaction can be triggered by viruses, medications, possibly vaccinations, and even cancer. The disease may develop suddenly and quickly progress to acute stage, but can be chronic. The more red blood cells are destroyed, the worse the prognosis.

With the acute development of YOGA, the dog is in a depressed state; for one to three days it may experience fever, shortness of breath, the gum color is pale pink, and the urine color is dark. There may be difficulties in moving. In the chronic form, the disease occurs in the form of remissions and relapses.

Diagnosis and treatment. YOGA diagnostics is based on clinical signs and blood test results. It is vital to begin treatment as quickly as possible with corticosteroids or other drugs that suppress the immune system. Blood transfusions are controversial not only because an overactive immune system will destroy fresh red blood cells, but because they sometimes even make the dog's condition worse. But there are rare situations in which blood transfusion is the only way to keep a dog alive.

The term "thrombocytopenia" refers to a decreased amount of small cells called platelets, or platelets, in the blood. Platelets are involved in blood clotting, so a lack of them can cause bleeding and bruising for any reason.

IOT is more common in females, regardless of whether the dog is spayed or not. This condition can develop after an infection, as well as as a result of the immune system’s reaction to certain medications. The first sign may be a bruise, accidentally noticed on an area of the body with less thick hair. An affected dog's stool is usually black due to bleeding in the gastrointestinal tract, and there is also blood in the urine. Some dogs experience nosebleeds.

Diagnosis and treatment of IOT. The veterinarian must differentiate thrombocytopenia from hemolytic anemia or other disease accompanied by bleeding. It is necessary to accurately count platelets per unit volume of blood. Treatment is usually with corticosteroids. Sometimes blood and platelet transfusions are used in combination with drugs that suppress the activity of the immune system. As with immune-mediated hemolytic anemia, some dogs develop a chronic form of the disease that requires long-term treatment drugs that suppress the activity of the immune system.

Neutropenia is a low level of neutrophils (a type of white blood cell) in the blood. Some drugs, such as sulfonamides and anticonvulsants, can trigger a condition in which the immune system suppresses the production of neutrophils. The disease responds well to treatment with corticosteroid drugs.

This form of arthritis develops due to the formation of synovium antigen-antibody complexes. Such arthritis may be accompanied by inflammation of the muscles (polymyositis) or inflammation of the nerve endings (polyneuritis). All forms of immune-mediated arthritis are treated with corticosteroids and other drugs that suppress the activity of the immune system. Some dogs with rheumatoid arthritis benefit from surgery to stabilize the affected joint.

This rare disease- inflammation of the membranes and blood vessels of the brain and spinal cord- may be associated with the formation of immune complexes. It is observed in young dogs of the following breeds: Akita, Beagle, Bernese Mountain Dog, Boxer, German Shorthaired Pointer. The dog suffers from intermittent pain in the neck and moves reluctantly. The attacks last for about a week. The use of corticosteroids improves the course of the disease.

Some autoimmune diseases attack skin cells. Solar dermatitis, also called discoid lupus, or erythematosis, is the most common. It occurs more often in certain breeds of dogs that live in sunny climates than in others. The disease is known as “collie nose” because collie (smooth and long-haired) and sheltie breeds are most susceptible to it. White American Shepherd and Siberian Husky dogs are also at risk of this disease.

Diagnosis and treatment. The diagnosis is made by visual examination. It responds well to treatment with corticosteroids; sun protection measures are required.

These diseases are rare. The most common of these is pemphigus foliaceus; reminds me at first allergic dermatitis with the development of a secondary bacterial infection affecting the face, nose, ears and skin around the eyes. Systemic (or acute) lupus erythematosus can cause similar skin problems and also affect internal organs. Other autoimmune skin diseases are observed in dogs, such as infectious-allergic and toxic-allergic exudative erythema, toxic-allergic epidermal necrolysis, and hereditary dermatomyositis.

One of the reasons for the attack of the body’s own lymphocytes on the body’s cells may be the similar structure of the body’s cells with the antigens of a bacterium or virus, i.e. the lymphocyte “confuses” its own cells with the antigens of infectious agents.

As a rule, the tendency to autoimmune pathology is genetic. Predisposing factors may include UV irradiation, infections, uncontrolled and unjustified use of immunostimulating agents, exposure to any chemical substances.

The nature of autoimmune diseases in cats has not yet been sufficiently studied. With pemphigus, disturbances in the animal's immune system lead to an attack on the animal's own epidermal cells. The destruction of skin cells and the release of their contents is clinically manifested by the formation of blisters.

The second reason may be a violation of the screening of autoreactive lymphocytes at the stage of their maturation. If a lymphocyte at the maturation stage is not able to distinguish the cells of the host body from foreign antigens, then such a lymphocyte must be destroyed. Sometimes the destruction mechanisms are disrupted.

Autoimmune antibodies: the body produces antibodies that attack healthy tissues and cells as if they were pathogenic.

Prolonged exposure to the sun.

Some breeds may have a hereditary predisposition.

Types of pemphigus

There are 4 types of pemphigus that affect dogs: pemphigus foliaceus, pemphigus erythematous, pemphigus vulgaris and pemphigus vegetans.

In pemphigus foliaceus, autoantibodies are found in the outermost layers of the epidermis and blisters begin to form on healthy skin. Erythematous pemphigus occurs in almost the same way as foliaceous pemphigus, but is less painful.

Pemphigus vulgaris is characterized by the formation of deeper ulcers, as antibodies accumulate in the lower layers of the epidermis. As for pemphigus vegetans, it affects only dogs and is considered the rarest variety.

Pemphigus vegetans resembles pemphigus vulgaris, but is much milder with the formation of less painful ulcers.

Clinical signs

Since exfoliative pemphigus is most common in cats, we will first look at the symptoms of this type of disease:

Generalized rashes of pustules (pictured), multiple crusts, small ulcers, redness and itching of the skin, including the head, ears and groin area are most often affected.

In other cases, large papules filled with cloudy liquid are observed.

Large cysts often form in the thickness of the skin.

In severe cases, the gums are also involved in the process, resulting in problems with teeth (even tooth loss).

Similarly, the nail beds are involved in the process, the animal’s claws begin to wobble and sometimes fall out. The process is very painful and causes great suffering to the animal.

Swollen lymph nodes; when palpated, the cat clearly shows signs of displeasure. The animal becomes apathetic, with increasing fever and lameness (if claws are involved). Note that all these signs are characteristic only for severe course process.

Secondary bacterial infection is possible due to the contamination of opened papules and ulcers with pyogenic microflora.

Autoimmune disease – this is a disruption of the immune system, in which an attack begins on the organs and tissues of one’s own body. In other words, the immune system perceives its tissues as foreign elements and begins to damage them.

The immune system is a protective network consisting 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. This is why the body rejects transplanted skin flaps, organs and blood transfusions. The immune system can malfunction due to either an inability to do its job or an overactive job.

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

The mechanism of autoimmune processes is similar to the mechanism of immediate and delayed types of allergies and boils down to the formation of autoantibodies, immune complexes and sensitized killer T lymphocytes.

The essence of autoimmune processes is that under the influence of pathogens of infectious and invasive diseases, chemicals, drugs, burns, ionizing radiation, and feed toxins, the 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-lymphocyte 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 can be organ diseases (encephalomyelitis, thyroiditis, diseases of the digestive organs caused by chronic intoxication and metabolic disorders) and systemic (autoimmune diseases connective tissue, rheumatoid arthritis). Can be primary or secondary. Primary arise as a result of congenital and acquired disorders in the immune system, accompanied by loss of tolerance immunocompetent cells to own antigens and the appearance of forbidden clones of lymphocytes.

A characteristic sign of autoimmune diseases is a long wave-like course.

The diagnosis of autoimmune diseases is made on the basis of anamnestic data . Clinical manifestations of the disease, hematological, biochemical and special immunological research 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 counts its own cornea foreign tissue and tries to tear her away.

The first reports of pannus appeared in areas with increased ultraviolet activity (in Austria and American state Colorado). Today, 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 severe and less treatable. This allows us to conclude that in the occurrence of this disease ultra-violet rays play an important role. 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 the metabolic processes are, the more actively the immune system tries to reject it.

This pathology is most common in dogs of such breeds 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 condition where a similar immune reaction affects the conjunctiva and third eyelid. Plasma is less likely to cause vision loss, but causes greater ocular discomfort.

Mechanisms of occurrence

Autoimmune pathology can be characterized as an attack by the immune system against the organs and tissues of the body’s own, resulting in their structural and functional damage. The antigens involved in the reaction, usually present in and characteristic of humans or animals, are called autoantigens, and antibodies that can react with them are called autoantibodies.

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

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

The essence of autoimmune processes is that under the influence of pathogens of infectious and invasive diseases, chemicals, drugs, burns, ionizing radiation, and feed toxins, the antigenic structure of the 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-lymphocyte 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 V damaged organs. Granular degeneration and necrosis are detected in parenchyma cells. 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 organ stroma, dystrophy is detected in the form of mucoid and fibrinoid swelling, necrosis and sclerosis. In the spleen and lymph nodes pronounced 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. Research into autoimmunity has led to significant advances in the diagnosis and treatment 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 of the 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 of the connective tissue with fibrinoid necrosis. Often affected and shaped elements blood.

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

Signs of autoimmune pathology, when autoimmune homeostasis is disturbed, may be the appearance of barrier antigens from tissues such as the lens of the eye, nervous tissue, testicles, thyroid, antigens that appeared under the influence of inadequate influences on the body of factors external environment infectious or non-infectious origin, genetically determined defects of immunocytes. Sensitization to autoantigens develops. The autoantibodies that interact with them can be conditionally divided into several groups: autoantibodies, causing damage cells, which underlies autoimmune diseases; autoantibodies themselves do not cause, but aggravate the course of an already existing disease (myocardial infarction, pancreatitis and others); autoantibodies are bystanders that do not play a significant role in the pathogenesis of the disease, but an increase in the titer of which may have diagnostic value.

Diseases associated with tissue damage by autoantibodies can be caused by:

antigens;
antibodies;
pathology of organs of immunogenesis.

Autoimmune pathology caused by antigens

The peculiarity 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 environmental factors, are perceived by the immunological apparatus as foreign.

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

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

Autoimmune pathology caused by antibodies

Has several options:

A foreign antigen entering the body has determinants similar to the antigens of the body’s own tissues, and therefore the antibodies formed in response to the foreign antigen “make a mistake” and begin to damage the body’s own tissues. The foreign antigen may subsequently be absent.
A foreign hapten enters the body, which combines with the body’s protein and antibodies are produced to this complex that are capable of reacting with each of its individual components, including its own protein, even in the absence of the hapten.
The reaction is similar to type 2, only a foreign protein enters the body, reacting with the body’s hapten, and the antibodies produced to 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 for the tissues of the body's own, which are formed 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 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 carditis, glomerulonephritis, rheumatoid arthritis, dermatomyositis, hemolytic anemia.

The pathogenesis of primary autoimmune pathology in humans and animals has a direct connection with genetic factors that determine the nature, location, and severity of the accompanying manifestations. Main role genes encoding the intensity and nature of immune responses to antigens - the genes of the major histocompatibility complex and the genes of immunoglobulins - play a role in the determinism of autoimmune diseases.

Autoimmune diseases can develop with the participation 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 recorded in diseases of a non-infectious nature. Increased immunological reactivity of horses with extensive wounds is known. At the large cattle ketosis, chronic feed poisoning, metabolic disorders, and vitamin deficiencies induce autoimmune processes. In newborns, they can occur through 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 a sharp increase in the permeability of biological barriers, tissue cells, pathologically altered proteins and substances associated with them enter the bloodstream, which become autoantigens.

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 that of antibodies to foreign antigens, since the body always produces normal anti-tissue autoantibodies, which 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.

Autoantibodies not only circulate in the blood, but at the end of the latent period, and especially during the height of radiation sickness, they bind so tightly to tissues internal organs(liver, kidneys, spleen, intestines), that even repeated washing of finely ground tissue cannot remove them.

Autoantigens capable of inducing autoimmune processes are also formed under the influence of high and low temperatures, various chemicals, as well as some medicines, used to treat animals.

Bovine autoimmunity and reproductive functions

The concentration of the best sires at state breeding enterprises and the use of their semen for artificial insemination have significantly increased the genetic potential of dairy herds. In conditions of widespread use of breeding males great importance has an assessment of the quality of their semen.

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

Immunological studies of the reproductive ability of male sires have revealed that overheating of the testes causes a disturbance in spermatogenesis, accompanied by the appearance of autoantibodies in the blood, and that their effect is due to an increase in the permeability of the blood-testis barrier.

There is also evidence that with age in breeding bulls, partial hyaline degeneration of the basement membrane, necrosis, and sliding of the seminiferous epithelium appear in some convoluted tubules of the testis.

Circulating antibodies to autologous sperm do not always and do not immediately inhibit spermatogenesis due to the presence of a powerful blood-testis barrier between the blood and seminiferous epithelial cells. However, trauma, prolonged overheating of the testes and the entire body, 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 consequence, to disruption or complete cessation of spermatogenesis. Most often, the process stops at the stage of round spermatids, but after prolonged 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 was found that intravenous administration suspension of foreign brain to a rabbit causes the formation of antibodies specific to the brain, which are able to specifically react with a suspension of the brain, but not other organs. These anti-brain antibodies cross-react with brain suspensions from other animal species, including rabbit. No antibody-producing animal was found to have any pathological changes own brain. However, the use of Freund's adjuvant changed the observed picture. Brain suspensions mixed with Freund's complete adjuvant, after intradermal or intramuscular injection 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, a suspension of rabbit brain 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 autoantigens, and the resulting disease 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 antibodies that precipitated thyroglobulin. Available great resemblance in the histological picture of experimental rabbit thyroiditis and chronic thyroiditis in humans.

Circulating organ-specific antibodies have been found in many diseases: anti-renal antibodies - in kidney diseases, anti-heart antibodies - for certain heart diseases, etc.

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

direct detection of free circulating or cellular antibodies;
identification specific antigen, against which this antibody is directed;
development of antibodies against the same antigen in experimental animals;
the appearance of pathological changes in the corresponding tissues in actively sensitized animals;
production of the disease in normal animals by passive transfer of serum containing antibodies or immunologically competent cells.

Several 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. The search for the virus has so far been unsuccessful, and it is very possible that a spontaneously occurring autoimmune disease in animals occurs. Antireceptor autoantibodies and their significance
in pathology

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

Research into the nature of atopic diseases, carried out over several decades, has indisputably proven the immunological nature of their trigger mechanism - the role of IgE in the biological release mechanism 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. We are talking about establishing the fact of the existence of autoantibodies to b-receptors in atopic asthma, placing this disease in the category of autoimmune pathology.

The question remains open about the cause and mechanism of the production of autoantibodies to the b-receptor, although, based on general ideas about the development allergic diseases, the appearance of autoantibodies can be explained as a consequence of dysfunction of suppressor cells, or, based on Erne's theory, by the fact that autoimmunity is a 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.

Unlike autoantibodies to b-adrenergic receptors, which are currently insufficiently studied, autoantibodies to acetycholine receptors have been studied quite well both experimentally and in the clinic. There is a special experimental model, showing an important pathogenetic autoantibody to acetylcholine receptors - experimental myasthenia gravis. When immunizing rabbits with acetylcholine receptor drugs, a disease resembling human myasthenia gravis can be caused. In parallel with the increase in the level of acetycholine antibodies, the animals develop weakness, reminiscent of myasthenia gravis in many clinical and electrophysiological manifestations. The disease occurs in two phases: acute, during which cellular infiltration and antibody damage to the end plate occur, and chronic. Acute phase may be caused by passive transfer of IgG from immunized animals.

Autoallergy

At different pathological conditions Blood and tissue proteins can acquire allergenic properties that are foreign to the body. Autoallergic diseases include allergic encephalitis and allergic collagenosis.

Allergic encephalitis occurs with 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 unique form of infectious autoallergic diseases. The autoantibodies formed in these cases cause a cytotoxic effect in the tissues; damage to the extracellular part of the connective tissue of a collagenous nature occurs.

Allergic collagenases include acute articular rheumatism, some forms of glomerulonephritis, etc. In acute articular rheumatism, corresponding antibodies have been detected. As a result experimental research The allergic nature of acute articular rheumatism was proven.

Many researchers believe that the pathogenesis of rheumatic carditis is similar to the pathogenesis of rheumatic carditis. Both of them develop against the background of focal streptococcal infection. In an experiment, when chromic acid was administered to animals, they developed renal autoantibodies and glomerulonephritis. Autoantibodies—nephrotoxins that damage renal tissue—can be obtained by freezing the kidneys, by ligating the renal vessels, ureters, etc.

Literature:

Pathological physiology of the immune system of domestic animals. St. Petersburg, 1998
Chebotkevich V.N. Autoimmune diseases and methods for their modeling. St. Petersburg, 1998
Immunomorphology and immunopathology. Vitebsk, 1996.
"Zootechnics" - 1989, No. 5.
"Animal Husbandry" -1982, No. 7.
Reports of VASKhNIL - 1988, No. 12.
Autoantibodies of the irradiated organism. M.: Atomizdat, 1972.
Modern problems of immunology and immunopathology. "Medicine", Leningrad branch, 1970.
Ilyichevich N.V. Antibodies and regulation of body functions. Kyiv: Naukova Dumka, 1986

Autoimmune diseases– a group of conditions characterized by “improper functioning” of the immune system - it does not “recognize” its tissues and produces cells (autoantibodies) against its own structures.

What is the reason for this unusual reaction?

This issue has not been fully studied. There are suggestions that the development of autoimmune diseases can be caused by a number of unfavorable factors: viral or bacterial infections, taking some medicines(sulfonamides, immunostimulants), any tumor diseases. An important role is assigned genetic predisposition body.

The most common autoimmune diseases in dogs are:

Autoimmune hemolytic anemia
Idiopathic thrombocytopenia
Systemic lupus erythematosus
Pemphigus vulgaris
Rheumatoid polyarthritis
Pseudoparalytic myasthenia

Autoimmune hemolytic anemia

The most common autoimmune disease in dogs, it is characterized by cells of the immune system attacking red blood cells, destroying them. The disease occurs in two forms: acute and chronic.

Symptoms. Manifestations acute form the following: general state The dog is depressed, its temperature rises, which lasts for two to three days, shortness of breath appears, the gums become pale pink, the urine darkens (becomes dark brown or bloody), and sometimes blood is found in the stool. Chronic form proceeds in waves - the subsidence of the disease (remission) alternates with exacerbation (relapse).

Idiopathic thrombocytopenia

A decrease in the number of platelets in the blood with impaired coagulation. Dogs of small and medium breeds are most prone to the disease during the first years of life. It has been noticed that females get sick more often.

Symptoms. The onset of the disease is sudden - small hemorrhages appear on the mucous membranes (conjunctiva of the eyes, oral cavity) and skin, in places of increased trauma. Sometimes massive bleeding from the nose, gums, intestines, vagina, and bladder develops. At the beginning of the disease, the general condition does not suffer, as the process progresses and blood loss increases, signs of anemia increase - the animal quickly gets tired, eats poorly, the skin and mucous membranes become pale, shortness of breath appears, and the heartbeat quickens.

Systemic lupus erythematosus (SLE)

A disease characterized by the involvement of many organs and systems simultaneously or gradually. Dogs of certain breeds are most prone to developing SLE (collie, sheltie, Siberian husky, Canadian-American white shepherd). Also, living in an area with a hot climate increases the risk of developing SLE.

Symptoms. The very first sign is nosebleeds, indicating thrombocytopenia. Then anemia develops - the skin becomes pale and sometimes jaundiced, weakness increases and fast fatiguability. The disease necessarily affects the kidneys, which leads to the appearance of protein and nitrogen in the urine. Often death occurs from renal failure. The joints are involved in the process, which causes an increase in temperature. As the disease progresses, the joints are destroyed. It should be noted that females aged 2-8 years get sick more often.

Rheumatoid polyarthritis

A disease characterized by inflammation of periarticular tissues, mainly large and medium-sized joints. The disease has a progressive course with frequent periods of exacerbation.

Symptoms. IN acute period the animal's condition is depressed, the temperature periodically rises. In the affected joints, there is limited movement, swelling, tension, and pain. The following joints are the first to be involved in the process: knee, elbow, hock, carpal. A specific syndrome is characteristic: with passive movements a sound appears, reminiscent of bone rubbing against bone. This means that the joints are being destroyed.

Pemphigus vulgaris

Autoimmune process skin-infecting and mucous membranes. Characteristic manifestations diseases - rashes in the form of blisters and the formation of extensive erosions.

Symptoms. The rash goes through several metamorphoses (transformations) - at the beginning erythema (redness) appears, in its place a bubble forms, which ruptures on its own. A non-healing erosion remains at the site of the ruptured bladder, which subsequently becomes covered with a crust. A secondary infection occurs very quickly, aggravating the general course of the disease.

The areas of skin and mucous membranes in transitional areas are most often affected. The first rashes are usually localized on the lips and skin of the nose. Subsequently, the rash appears on the oral mucosa and conjunctiva of the eyes. In such sick animals, it comes from the mouth putrid smell, salivation of a purulent-foamy nature is noted. The area around the anus, vaginal mucosa and prepuce are often affected. Most Frequent skin lesions– popliteal area, interdigital spaces, skin at the base of the claws.

Pseudoparalytic myasthenia

An autoimmune disease that rapidly attacks the nervous and muscular system. This disease is characterized by rapid fatigue and pathological weakness of certain muscle groups - mainly respiratory and muscles innervated cranial nerves. Large breed dogs are most prone to developing myasthenia gravis.

Symptoms. After a short and insignificant load, the sick animal weakens, has difficulty standing on its feet, sinks, and moves in small steps, more like hare jumps. Characteristic appearance: stiff parts of the body, arched back, trembling muscles. After a short rest, all changes disappear.

Half of affected dogs have lesions digestive system in the form of difficulty swallowing, increased salivation, vomiting with mucus, and a cough. These manifestations of myasthenia gravis are caused by paresis of the esophagus.

Treatment

Treatment of all autoimmune diseases consists of prescribing massive doses of hormones (glucocorticoids) until relief acute manifestations illness, followed by transition to maintenance doses. Good effect prescribes medications that suppress excessive activity immune system. This group of diseases is difficult to treat. The prognosis, in many cases, depends on timely seeking medical help.

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