Diagnosis and treatment of autoimmune skin diseases in dogs and cats. "autoimmune diseases of animals"

Violations immune system– a serious threat to your dog’s health

What is the immune system

The term “Autoimmune disease” remains in use among breeders, owners show dogs, as well as in the veterinary community. In particular, diseases caused by disorders of the immune system pose a problem for many purebred animal lovers. Sometimes the abbreviation AIZ is used to designate (A)uto(I)immune (Z)diseases.

The immune system is an amazing defense network made up of white blood cells, antibodies and other components involved in fighting infection and rejecting foreign proteins. Like a police patrol patrolling the body, this system distinguishes “friend” cells from “non-self” 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, like any other, can malfunction due to either an inability to do its job or an overactive performance of it.

Sometimes children (as well as Arabian foals) are born with severe combined immunodeficiency(SCID). In addition, some viruses, such as feline and simian immunodeficiency virus and human immunodeficiency virus (HIV), cause species-specific acquired immunodeficiency syndrome (AIDS). In all of these diseases, a defective immune system fails to protect the body, leaving it vulnerable and open to attack by opportunistic pathogens.

Autoimmune diseases are the opposite type of immune system disorder. In this case, the immune system loses the ability to recognize “its” markers, so it begins to attack and reject the tissues of its own body as foreign. In this case, there may be either damage to a specific tissue type, such as red blood cells, or a generalized disease, such as systemic lupus.

What causes a short circuit in the immune system, causing it to reject normal tissue? There are many theories, but the final answer is: "It is unknown." Jean Dodds, a veterinarian who studies immunology, believes that multivalent modified live vaccines cause overstimulation of the immune system. Other authors blame environmental pollution or food preservatives such as ethoxyquin, an antioxidant found in most dog foods. There is convincing evidence for the role of genetic factors in the development of autoimmune diseases in many animal species. Some cases develop spontaneously and are accompanied by damage to the kidneys, lungs or thyroid gland.

Firstly, there is the risk of serious illness or even death of the affected dogs, which can lead to a very large loss if we are talking about your winning bitch or high-quality stud dog. Second, most autoimmune diseases are treated with very high doses of corticosteroids or other immunosuppressive drugs that suppress the immune response and are similar to the drugs kidney recipients take to suppress rejection. Steroids suppress a female dog's reproductive cycle, sometimes making her unable to reproduce. If pregnancy occurs, daily use of medications may cause birth defects in puppies, including cleft palate and limb malformations, as well as premature birth or spontaneous abortion. Since there is good reason to believe that such diseases are inherited and pose a risk to the bitch and her litter, such dogs should not be allowed for breeding. What can be said about breeding close relatives - littermates, mother, father, half-siblings - sick dogs? Should a breeding that has produced one or more sick puppies be repeated? To confirm or reject the hereditary nature of any disease with a suspected genetic component, a series of test crosses must be performed. As far as we know, no official recommendations have been developed that could be relied upon when making such a decision, but you can follow a very obvious algorithm:

1. Breeding to any dog ​​or bitch with a diagnosed autoimmune disease should not be recommended.
2. In the event that two or more puppies from the same litter are diagnosed with any autoimmune disease, it is not advisable to breed these two specific dogs or dogs from the same line.
3. Finally, you should avoid breeding two dogs if both dogs have close relatives with an autoimmune disease.

Unfortunately, due to the subtle nature of autoimmune diseases, symptoms may become apparent in offspring after your suspect dogs have completed their breeding careers. Until more concrete evidence is available, veterinarians will have to rely on the integrity of breeders to research pedigrees and allow only the best of the breed to be bred.

Autoimmune hemolytic anemia

Anemia is not a disease, but a clinical sign that is a decrease in the number of red blood cells or hemoglobin content, reducing the ability of the blood to carry oxygen. Anemia can be caused by blood loss, decreased production of new red blood cells, or increased destruction of red blood cells, known as hemolytic anemia.

The spleen and the rest of the immune system strive to rid the body of old, diseased, or damaged red blood cells, which is their normal function. If affected large percentage cells and they are destroyed faster than they are replenished, AIHA develops and the animal develops external signs of the disease.

Clinical signs of AIHA usually develop gradually and progress, but sometimes an apparently healthy animal suddenly declines and experiences an acute hemolytic crisis. Symptoms are usually associated with a lack of oxygen: weakness, severe lethargy, lack of appetite, increased frequency of heart rate and breathing. Possible heart murmurs and pallor of the mucous membranes (gums, eyelids, etc.). In more severe cases, fever and jaundice (icterus) develop, i.e. yellow coloring gums, whites of eyes and skin. This is due to the accumulation of bilirubin, one of the breakdown products of hemoglobin.

Diagnosis is usually made by these clinical signs and by CBC results indicating anemia; in this case, red blood cells are often found to be irregularly shaped or stuck together. To confirm the diagnosis, a Coombs test can be performed. The main treatment for any autoimmune disease is corticosteroids. At the beginning of treatment, very high immunosuppressive doses are used to induce remission, and then the dose is slowly reduced over many weeks or months to a low maintenance dose. Most affected animals require lifelong steroid therapy and remain at risk of relapse.

If steroids alone are not enough, more powerful immunosuppressive drugs can be added: Cytoxan (cyclophosphamide) or Imuran (azathioprine). These are very effective chemotherapy drugs and the dog should remain under close monitoring due to the possibility of side effects, including due to the likelihood of a decrease in the number of leukocytes in the blood.

In cases that cannot be treated, splenectomy can be recommended - surgical removal of the spleen. Positive effect This intervention is due to two mechanisms: the dog produces fewer antibodies against red blood cells and the main organ responsible for their destruction is removed. An animal without a spleen can live a completely normal life.

Blood transfusions are rarely used. Adding a foreign protein may actually make the crisis worse by increasing the production of bilirubin and other waste products that the liver must process and suppressing normal reaction bone marrow for anemia. At life threatening anemia, blood transfusion is possible (after checking for compatibility using a crossover test) in combination with immunosuppressive therapy.

Immune-mediated thrombocytopenia

Treatment is the same as for AIHA - high doses of corticosteroids and the addition of cyclophosphamide or vincristine if corticosteroids are ineffective. Possible removal of the spleen; however, the surgical risk is higher due to worse blood clotting with IOT. In some cases, transfusion of fresh whole blood or platelet-rich plasma.

The prognosis for AIHA is cautious. With the rapid development of a crisis condition, animals often die before the start of active therapy, while in other cases it is not always possible to achieve remission or maintain it. The prognosis for IOT is usually good, although ovariohysterectomy is recommended once the platelet count has normalized. This reduces the risk uterine bleeding in case of relapse. Affected males and females should not be used for breeding due to the effects of steroids on the offspring and the risk of hereditary transmission of susceptibility.

Autoimmune skin diseases

Autoimmune skin diseases belong to the group of infrequent or rare diseases. Making a diagnosis can be difficult, especially for a general practitioner who has seen no more than 1-2 cases in their entire career. Diagnosis of such diseases usually requires skin biopsy and immunofluorescence staining, and the prognosis for recovery varies. Corticosteroids are considered the main treatment.

"Pmphigus complex"- a group of four autoimmune skin diseases characterized by the appearance of “vesicles” or “vesicles” (blisters), erosions and ulcers. At pemphigus vulgaris (pemphigus vulgaris) lesions are usually located in the oral cavity and at the skin-mucosal interface, that is, between the hairy skin and the mucous membrane. These areas include the eyelids, lips, nostrils, anus, prepuce and vulva. Skin lesions in the groin or armpits also occur. The bubbles are thin, fragile and break easily. The skin lesions are described as red, weeping, ulcerated plaques.

And when "pemphigus vegetans" the affected areas are thick, irregular in shape, and proliferate to form vegetative lesions with exudation and pustules. It is believed that this is a benign form of pemphigus vulgaris.

Pemphigus foliaceous– a rare disease that affects the oral cavity or areas at the border of the skin and mucous membranes. Bubbles form briefly; the most common symptoms are redness, crusting, flaking and hair loss. Usually pemphigus foliaceus It begins on the face and ears and often spreads to the limbs, paw pads and groin. Secondary skin infections often develop; in severe cases, fever, depression and refusal to feed are possible.

Erythematous pemphigus ("Pemphigus erythematosis") clinically it appears leaf-shaped and often develops on the nose. Ultraviolet radiation aggravates this form of pemphigus and may lead to the misdiagnosis of solar nasal dermatitis (“collie nose”). This form is considered a benign form of pemphigus foliaceus. The term "bullous pemphingoid" is similar to the term "pemphigus" (pemphigus), according to clinical course These diseases are also similar. At the same time, blisters and ulcers of the same type can be found in the oral cavity, at the border of the skin and mucous membranes, in the armpits and in the groin. Differentiation is only possible with the help of a biopsy. Evaluation of the blebs is critical to diagnosis and because they rupture soon after formation, the dog often has to be admitted to the hospital and examined every 2 hours until a biopsy can be obtained.

Left: Pemphigus in a dog.
On the right is Pemphigus in a cat.

Discoid lupus erythematosis is believed to be a benign form systemic lupus and is an autoimmune dermatitis on the face. Most often found in collies and shelties; more than 60% of sick dogs are females. The lesion is often described as a "butterfly silhouette" on the bridge of the nose; it should be differentiated from solar nasal dermatitis and erythematous pemphigus.

Finally, a syndrome similar to Vogt-Koyanagi-Garada syndrome (VKG) is exclusively rare disease, possibly of an autoimmune nature, leading to depigmentation and concomitant eye damage. The black pigments of the nose, lips, eyelids, paw pads and anus fade to pink or white, and acute uveitis (inflammation of the eyes) develops. If treatment is started promptly, blindness can be prevented, but lost pigment is usually not restored. As you can see from the above descriptions, many autoimmune diseases have similar manifestations, except for discoid lupus, they do not have a breed, gender or age predisposition.

As with other autoimmune diseases discussed previously, the main goal of treatment is to suppress the body's immune response large doses systemic glucocorticoids. If steroids are ineffective, more powerful drugs such as Cytoxin or Imuran are prescribed.

Gold preparations have been proposed for the treatment of diseases from the pemphigus or pemphingoid group. In cases of nasal depigmentation, tattooing the affected areas helps prevent sunburn and the possible development of squamous cell carcinoma.

The prognosis for discoid lupus is usually good, but can vary for other diseases. Many dogs with ICH are euthanized due to blindness. Breeding sick dogs is not recommended. Currently, there is insufficient information about the heritability of autoimmune skin diseases.

Systemic lupus erythematosus

Systemic lupus erythematosus (SLE) (or simply lupus) is a classic example of a multisystem autoimmune disease. Lupus is often referred to as the “great imitator” because it can present like almost any other disease. Symptoms of SLE can be acute (rapid development) or chronic and usually cyclical. Intermittent fever that does not respond to antibiotics is one of the distinguishing clinical features; another sign is a stiff gait or lameness that moves from one limb to another (polyarthritis, see below). Other things possible signs include hemolytic anemia or thrombocytopenia, leukopenia (low white blood cell count), or symmetrical dermatitis, especially on the dorsum of the nose (butterfly-shaped).

In SLE, two other organ systems may be affected. Polymyositis (inflammation of many muscle groups) causes gait changes, exhaustion muscle mass, fever and pain, as well as behavioral changes common in dogs in pain. Inflammation of the glomeruli, functional units kidneys, causes a condition called glomerulonephritis. It leads to loss of protein in the urine and ultimately to kidney failure.

As with the diagnosis of other similar diseases, first of all it is necessary to make a complete clinical analysis blood, biochemical analysis serum and urine analysis. The definitive diagnosis of SLE is the determination of antinuclear antibodies (ANA). This method reveals positive cases with greater consistency than older methods, and its results are less affected by time and steroid therapy. Only a few ml are required for analysis. serum, which must be sent to a veterinary laboratory that specializes in analyzing samples from animals.

Therapy is based on the anti-inflammatory and immunosuppressive effects of corticosteroids or more powerful drugs - Cytoxan and Imuran. However, due to the wide variety of lupus manifestations, individualized treatment may be required on a case-by-case basis. If infection develops due to a decrease in white blood cells and immunosuppressive therapy, antibiotics should be prescribed. Can be used as a maintenance treatment for dogs with kidney dysfunction. infusion therapy and low protein diet.

The prognosis for SLE is guarded, especially when complicated by renal disorders. Severe generalized infections of the kidneys (pyelonephritis), joints (septic arthritis) or blood (septicemia) are usually incurable and develop late stage diseases.

Polyarthritis

Immune-mediated polyarthritis occurs both in SLE described above and independently. This classification includes several different specific diseases, however, all the main symptoms are similar. TO typical signs include high fever, tenderness and swelling of the joints, as well as lameness that moves from one limb to another. In some cases, enlarged lymph nodes are found. In deforming (erosive) arthritis, for example, rheumatoid arthritis (RA), radiography of the joints is informative, but in non-deforming (non-erosive) types it does not show changes. Blood test results may be normal, elevated, or decreased.

In uncomplicated immune-mediated polyarthropathy, remission can be achieved with corticosteroids in approximately half of cases. In the remaining cases, cytotoxin or imuran is prescribed to induce remission, and then steroids are used to maintain it. The prognosis for these diseases, with the exception of rheumatoid arthritis, is usually good. RA is more common in small breeds.

Recently, researchers have begun to explore the possible role of the immune component in many well-known diseases. Endocrine disorders(eg, hypothyroidism or diabetes) may be caused by the immune system rejecting hormone-producing cells. Keratoconjunctivitis sicca (KKS or dry eye syndrome), which develops due to the cessation of tear production, can be treated with cyclosporine, which is used to suppress rejection. Chronic active hepatitis (liver disease) may also have an immune basis. In these and many other areas of medicine, research is currently underway to find possible connections to the complex world of autoimmune diseases.

ST. PETERSBURG ACADEMY OF VETERINARY MEDICINE

Department of Pathological Physiology

Abstract on the topic:

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, chemical substances, 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-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 in damaged organs. Granular degeneration and necrosis are detected in parenchyma cells. In the 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 of the thyroid gland are observed, including mononuclear infiltration, destruction 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 connective tissue with fibrinoid necrosis. 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 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.

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

1) antigens;

2) antibodies;

3) 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. If the hematoparenchymal barriers are damaged (trauma, surgery), these primary antigens enter the blood, stimulate the production of antibodies, which, penetrating through 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:

1. 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.

2. A foreign hapten enters the body, which combines with the body’s protein and antibodies are produced to 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 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 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 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. The main role in the determinism of autoimmune diseases is played by genes encoding the intensity and nature of immune responses to antigens - the genes of the major histocompatibility complex and the genes of immunoglobulins.

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 sharp increase Through the permeability of biological barriers, tissue cells, pathologically altered proteins and substances associated with them enter the bloodstream and 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.

Autoantigens that can induce autoimmune processes are also formed under the influence of high and low temperatures, various chemicals, as well as some medications 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. 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-heart antibodies in certain heart diseases, etc.

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) identification of the specific antigen against which this antibody is directed;

3) development 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 the disease in normal animals through 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 various hormone receptors have been 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 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. It's about 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 of 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 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

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 are nephrotoxins that damage kidney tissue, can be obtained by freezing the kidneys, by ligating the renal vessels, ureters, etc.

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 in damaged organs. Granular degeneration and necrosis are detected in parenchyma cells. In the 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. The spleen and lymph nodes show hyperplasia and 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 of the thyroid gland are observed, 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. 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 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 effects on the body of environmental factors of 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 of an 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 is divided into primary and secondary. Autoimmune diseases are primary.

Autoimmune diseases include diabetes, chronic thyroiditis, atrophic gastritis, ulcerative colitis, primary cirrhosis, 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. The main role in the determinism of autoimmune diseases is played by genes encoding the intensity and nature of immune responses to antigens - the genes of the major histocompatibility complex and the genes of immunoglobulins.

Autoimmune diseases can be formed with the participation of various types of 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 may prevail. (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. In 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 firmly 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. Given the widespread use of breeding males, assessing the quality of their semen is of great importance.

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 long acting antibodies stops and spermatogonia division 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 of a 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. 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 Freund's complete 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, 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 of thyroglobulin obtained from other animal species resulted in the production of antibodies that precipitated thyroglobulin. 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-heart antibodies in 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 of the specific antigen against which the 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 the receptors of various hormones have been quite well studied in certain types of endocrine pathology, in particular in diabetes and 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 recent years there has been an increased interest in other antireceptor autoantibodies - antibodies to neurotransmitters; 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.

Research into the nature of atopic diseases, conducted over several decades, has indisputably proven the immunological nature of their trigger mechanism - the role of IgE in the mechanism of release of biologically 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 of 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 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 classical 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

In various 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 of experimental studies, 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 diseases that are characterized by an excessive reaction of the immune system to the body’s own cells and tissues, the so-called target cells. In dogs and cats of autoimmune origin include diseases of the pemphigoid complex (pemphigus foliaceus, bullous pemphigoid, vegetative and erythematous pemphigus), systemic lupus erythematosus, discoid lupus erythematosus, auricular polychondritis, vasculitis, cold agglutinin disease.

Pemphigus foliaceus

In this disease, the target cells are the intercellular substance in. As a result, a split occurs between the papillary and stratum corneum. Externally this process manifested by education. Pustules are usually localized in the muzzle and ears, large in size, symmetrically located. In the absence of pustules, an incorrect diagnosis is often made. Systemic reactions may occur - anorexia, fever, apathy. The diagnosis is confirmed using.

Pemphigus vulgaris

In this disease, the splitting occurs mainly between the basal and stratum corneum of the epidermis. Clinically, pemphigus vulgaris manifests itself as vesicles and ulcerations on the oral mucosa and mucocutaneous border. Since ordinary pemphigus occurs with the appearance of ulcers in the skin, the disease is often severe and can threaten the life of the animal. If pemphigus vulgaris is suspected, calicivirus in cats and ulcerative gingivitis should be excluded. The diagnosis is made based on histological examination of the skin. For of this disease characterized by the presence plasma cells on basement membrane, which are arranged in the form of “tombstones”.

Bullous pemphigoid

Occurs in dogs; this disease is not typical for cats. It is manifested by the appearance of short-term blisters with purulent contents, then they ulcerate. Lesions are localized on the muzzle, mucocutaneous border, abdomen, groin area, limbs. The analysis is based on a biopsy of the lesions.

Pemphigus vegetans

It is extremely rare. It appears in a milder form than other forms of pemphigus (multiple papules and pustules). It is important to exclude skin neoplasms. Diagnostics includes histological examination skin.

Erythematous pemphigus

It is considered a mild form of pemphigus. Often the lesions are localized only in the nose area. There is depigmentation of the nose, crusts, ulcers, blisters on the back of the nose and in the bridge of the nose.

For all types of pemphigus, Nikolsky's sign can be positive. Externally it manifests itself as desquamation of the epithelium at the slightest touch. This is due to the fact that the epidermis delaminates and the connection between the layers is disrupted.

Systemic lupus erythematosus

With this disease, antinuclear antibodies are produced that affect cells of all body systems - blood, joints, skeletal muscles, lungs, kidneys, organs gastrointestinal tract, skin, central nervous system. Unlike systemic lupus erythematosus, discoid lupus primarily affects the skin.
For lupus skin lesions usually symmetrical, localized on the muzzle - nose, ears, periorbital region, mucocutaneous border. First, foci of depigmentation appear, then erythema appears, and subsequently ulceration of the skin in this area occurs. In systemic lupus erythematosus there are following symptoms: hemolytic anemia, thrombocytopenia, fever, polyarthritis.

To diagnose lupus, there are specific tests - the antinuclear antibody test and the lupus erythematosus test. Also, for deep dermatoses, a skin biopsy is informative. If systemic lupus erythematosus is suspected, a comprehensive diagnostics to assess the involvement of other organs and systems in the pathological process.

Auricular polychondritis

The target cells in this disease are cartilage cells. Anti-collagen antibodies are formed in the body. Externally, the disease manifests itself mainly as damage to the ears - swelling, pain, redness occurs, which, if left untreated, leads to deformation of the cartilage tissue. Fever and damage to the connective tissue of the nasal passages may also occur. A biopsy of the affected tissue is required to confirm the diagnosis.

Vasculitis

When affected blood vessels, the disease causes a narrowing of the lumen of blood vessels. Due to insufficient blood supply, tissue death gradually occurs in the peripheral parts of the body. Most often, the edges of the ears, paw pads, tip of the tail, scrotum, and lips are affected. Diagnosis is made based on clinical signs and confirmed by skin biopsy.

Cold agglutinin disease

The disease is based on reaction Ig M on red blood cells. It is characteristic that red blood cells react with immunoglobulins only when the temperature drops. Thus, the disease manifests itself more often in the cold season, affecting distal parts of the body: ears, limbs, nose, tail, scrotum. Depigmentation is observed in these areas, and necrosis may develop.

Vitiligo

Melanocytes in the epidermis are affected. Externally it manifests itself as loss of pigment in various parts of the body. The area of ​​the nose, lips, and paw pads is mainly affected. Predisposed to disease Siamese cats. Effective treatment not currently developed. Spontaneous return of pigment may occur.

Treatment

Treatment of all autoimmune dermatoses in cats and dogs except vitiligo is based on immunosuppressive therapy. For this purpose, drugs are prescribed, cyclosporine, azathioprine, chlorambucil. The drugs are used both individually and in combination. In addition to immunosuppressive therapy, symptomatic treatment– antibiotic therapy for the accumulation of secondary microflora, drugs that improve peripheral blood supply in case of vasculitis.
The prognosis for autoimmune dermatoses depends on the involvement of other organs and systems in the pathological process. It is important to start treatment as early as possible, this increases the chances of successful outcome, which is why it is so important to make a timely appointment with veterinarian and do not self-medicate your pet.

Veterinary & Aquatic Services Department, Drs. Foster & Smith.

* This page is a continuation of the article The cat's immune system.

The immune system does not always work properly. Sometimes this results in a false positive (autoimmune reaction), in other cases the body reacts too much (hypersensitivity), and sometimes there is no reaction at all (immunosuppression and immunodeficiency).

Autoimmune reaction.

In the case of an autoimmune reaction, the immune system mistakenly perceives some part of the body as foreign and begins to attack it. Both T and B cells may be involved in the autoimmune response. What causes this disorder?

In some cases, the genetic characteristics of the cat play a major role in the development of autoimmune disorders. Some disorders are more common in some breeds than others.

Some medications can change the molecular composition of cells. Some drugs attach to red blood cells, after which the immune system begins to perceive them as foreign, the body attacks the red blood cells, causing autoimmune hemolytic anemia.

As with drugs, in some cases the antigen-antibody complex can attach to cells, causing the same type of reaction - the body attacks the cells as if they were foreign. Sometimes their destruction can be accompanied by severe inflammation. This type of autoimmune reaction is believed to contribute to the development of rheumatoid arthritis in cats. Errors in the “training” of T and B cells lead to the fact that they cannot distinguish native cells from foreign ones.

Many scientists are studying autoimmune reactions and their differences in different types animals. In the future, there is hope to better understand the causes of such disorders in order to prevent and treat them.

There are two types of autoimmune diseases - when antibodies are directed to a specific organ, and those in which several areas of the body are affected.

Types of autoimmune diseases in cats.

• Exfoliative (leaf-shaped) pemphigus (pemphigus foliaceus) is a skin disease;
• Myasthenia gravis is a nervous disorder;
• Hemolytic autoimmune anemia;
• Chronic progressive polyarthritis;
• Systemic lupus erythematosus;

Hypersensitivity.

Immune system hypersensitivity results in an overreaction to stimuli. In addition to T and B cells, various others can be activated during an immune response. They produce chemicals such as histamines that affect many organs in the body. In hypersensitivity, a cat's body produces too many antibodies, the wrong type of antibodies, too many antigen-antibody complexes, or antibodies to proteins that are not actually foreign. Additionally, excessive numbers of cells may be activated to produce histamine and other chemicals. There are four main types of hypersensitivity.

Immunosuppression (immunosuppression) and immunodeficiency.

Immunodeficiency may be caused by genetic defects, inherent in certain breeds of cats. Some may lead to its development viral infections(for example, feline immunodeficiency virus). Newborn kittens that do not receive enough colostrum are susceptible to immunodeficiency, and, therefore, to a greater extent are at risk of serious infectious diseases. Poor nutrition, lack of vitamins A, E, selenium, protein and calories can lead to a suppressed immune system.