Pathology associated with disruption of the immune system or vasculitis in a dog: how to recognize and how to treat inflammation of the inner layer of blood vessels. Cutaneous vasculitis

If the owner has discovered very strange sores on the tips of his beloved pet’s ears, then he should under no circumstances be negligent about this kind of problem. It should not be left without due attention at all.

For every dog, its ears are perhaps the most the main body feelings, we can with absolute confidence call them an important analyzer, therefore, every dog ​​owner must ensure that his ears and hearing are in perfect order.

At home, the dog’s ears can be treated with hydrogen peroxide to improve the pet’s living conditions and diet.

Vasculitis

Even the most inattentive owner can find sores, ulcers and scabs on the tips of his dog’s ears. Vasculitis can be noticed immediately, because it is characterized not only by the appearance of sores, but also by hair loss and redness of large areas skin pet.

Vasculitis is an inflammation of blood vessels, leading to quite serious damage to their walls. This pathology causes an autoimmune reaction, during which the protective mechanisms operating in the body begin to actively destroy its own cells, and subsequently tissues.

Causes

This disease is caused by:

1. Various types of infections.
2. Reaction to medications. Often, owners try to cure their pets on their own, stuffing them with a variety of medications. Quite often, dogs are given vaccines.
3. Autoimmune diseases (for example, neoplasia - pathological growth of tissues in the body).

Vasculitis is not a common disease, but it affects young and old animals equally.

Signs of the disease

From the moment this pathology appears in the dog’s body, it occurs throughout its entire body. To a greater extent, ulcers may occur at the tips of the ears, at the site of which bleeding appears.

1. The affected area begins to swell, although signs of inflammation may not be visible.
2. The dog may experience feverish conditions.
3. The animal experiences pain, its appetite noticeably decreases and progressive weight loss occurs.

Diagnostics

• Analysis of urine.
• Taking a complete blood test.
• Blood biochemistry.

If vosculitis is diagnosed it is impossible to do without radiography and ultrasound examination – research of the condition is necessary internal organs animal. How more methods diagnostics will be used, the faster it will be identified main reason the occurrence of pathology.

Therapy

The main decision in the treatment of vosculitis is to determine the root cause that led to the abnormal development of auto immune system, and its further elimination. Treatment of this disease involves the use of drugs such as:

• Corticosteroids (Pentoxifylline, Prednisolone).
• Tetracycline antibiotics and nicotinic acid(niacin) (Dapsone, Sulfasazaline).
• Immunosuppressants – cyclosporines (Imuran).

Treating a pet requires a combined approach. Some dogs can get rid of vosculitis fairly quickly, while others live with this pathology throughout their lives. Relapses of the disease cannot be ruled out either.

Disease prevention

The owner should periodically check the blood condition of his pet. It is almost impossible to cure vasculitis at home on your own.

Allergic reaction

The cause of sores on the tips of a dog’s ears can be a banal allergy to care products, medications and food

Treating sores on the tips of dogs' ears at home

It is not always possible for an owner to take his pet to veterinary clinic, for example, this happens if a dog lives in the country. In this case, first aid can be provided to your pet as follows:

1. Buy at a pharmacy Birch tar and actively lubricate the tips of the dog’s ears.
2. The previous option can be replaced with Vishnevsky ointment.
3. Also, the affected areas are washed with a solution of furatsilin (2 tablets dissolve in a glass of warm boiled water), and then they are sprinkled with streptocide on top.
4. Review your dog's diet, eliminating porridge and potatoes for a while.
5. Treat with hydrogen peroxide and burn with brilliant green (after all, it is possible that the pet could simply have gotten into a fight with other dogs).

It would be best to show your dog to a specialist, such as a veterinarian.

Normally, the dog's ears should be clean (a small amount of wax is allowed), even in color and free of any scabs, crusts or sores. When a dog has crusts on the tips of its ears, it means there is a disease. It is unacceptable to pick off scabs or wet them with water. Correct treatment is only possible when determining the cause of the problem.

Otodectosis (ear mites)

The disease occurs more often in indoor dogs who come into contact with cats that have free access to the street; or those living on the street and in contact with stray animals. Purebred pets have less strong immunity and therefore are more often affected by ticks than mongrel dogs.

Additional symptoms of otodectosis are as follows: severe itching and the accumulation of a black-brown mass (mite waste) in the ear canals. Treatment of the disease includes the following steps:

• cleaning ears with cotton swab, moistened with hydrogen peroxide;
• burying special drops against ear mites;
• treating crusts with chlorhexidine or brilliant green to prevent infection.

If the disease is not treated, then inflammation gradually develops, which spreads to the brain and leads to the death of the pet.

To speed up your pet's recovery, it is necessary to increase the duration of walks and provide the most balanced diet.

Vasculitis

In the case of this disease, in addition to the formation of crusts at the end of the ear, the dog also experiences hair loss in the affected area. Also, in most cases, intense redness appears on most of the inside ear.

Vasculitis is an inflammation of the walls of blood vessels that develops due to an improper immune response of the body to own fabrics. The ears are the first to be affected. The disease cannot be called common, but it can occur in animals of any age. Crusts on the tips of a dog's ears when the disease occurs are formed due to the fact that the walls of the blood vessels are damaged and numerous small wounds appear, which are quickly covered with a crust, usually brown in color.

Treatment of vasculitis is complex. For some animals it is a course, after which the problem is completely eliminated; and for others, lifelong therapy is required. You should also take into account the fact that the disease can recur after the outbreak is eliminated. Because of this, the condition of a dog that has encountered vasculitis requires constant monitoring.

Dermatosis

A condition that occurs for a variety of reasons, especially in dogs with floppy ears. In the absence of treatment, in addition to crusts, baldness of the ears appears. If at this moment the animal does not receive help, then the disease spreads to its face.

With this disease, the formation of scabs is associated with the excessively rapid death of skin cells, which is why the lower layer is not protected. As a result, crusts are formed such as at the site of an abrasion.

Photo of a dog with crusts on the tips of its ears

Lichen

The lesion can occur on any part of the body, including the ears. Most lichens are contagious to humans. With the disease, not only the appearance of crusts is observed, but also cracks and ulcers. . Because of the itching, the dog vigorously rubs the affected ear with its paw, which in most cases spreads the disease to it.

Injury

Dogs with long floppy ears are often injured. When they are serious, they are noticed by the owner immediately; and minor ones, in which there is no hematoma or bleeding, are usually not detected quickly. They become noticeable only if they are in place minor scratches or cuts, a translucent yellowish crust forms.

If it is accidentally torn off, there is almost always no bleeding, and only a clear, slightly yellowish liquid is released. For treatment, simply treat the affected area with an antiseptic. After the wounds heal, the scabs will fall off. For this reason, crusts on the tips of a dog's ears may appear regularly.

Allergy

Allergies often cause dry crusts to appear all over the animal’s body, including the tips of the ears. With this phenomenon, the pet begins to discharge in large quantities tear fluid and sulfur secretion from the ears. General swelling is also possible. In severe cases, signs of allergy include drooling and loss of coordination. For emergency assistance at home you can use suprastin. The dosage is calculated based on the weight of the animal.

Crusts on the tips of a dog's ears are rarely a signal dangerous disease, which threatens the life of the animal, but they cannot be considered the norm. To restore your pet’s health, therapy must be timely.

Any health problems that arise in dogs should not be ignored by owners. Many diseases manifest themselves in various changes on the skin. But often the causes of such conditions have a deeper nature.

One of the pathologies associated with disruption of the immune system in dogs is vasculitis. It is accompanied by inflammatory processes in blood vessels and can be both local and systemic in nature. This serious illness, requiring constant and long-term treatment. The sooner vasculitis is detected, the easier it will be to combat the pathology.

What is vasculitis

Vasculitis - common name for a group of diseases in which inflammation of the inner layer of blood vessels occurs, eventually leading to damage to their walls. The inflammatory process starts due to the fact that the body’s defense mechanisms begin to attack its own cells and produce antibodies against them. The dog’s body struggles with viral and other infections, and in this case they come under attack healthy cells and the vessels become inflamed.

Classification of the disease

By origin:

• Primary- occurs as an independent disease.
• Secondary- develops against the background accompanying pathologies which lead to vascular damage.

According to the severity of the course, vasculitis can be:

• light;
• moderate;
• heavy.

Depending on which vessels become inflamed, forms of vasculitis are distinguished:

• capillaritis;
• arteriolitis;
• arteritis;
• phlebitis.

Depending on prevalence:

• systemic necrotic;
• vasculitis of individual organs.

Causes

The most common trigger for the development of vasculitis is viral diseases resulting from vascular damage. The exact reasons why the immune system begins to destroy its own healthy cells have not yet been studied.

Other causes of vasculitis in dogs may include:

• use of potent drugs;
• incorrectly selected therapy using medications that are incompatible with each other;
• reaction to the vaccine;
• tumor formations;
• neoplasia (pathological tissue growth);
• renal failure;
• chronic joint diseases;
• systemic lupus.

What parts of the body does the disease affect?

Vasculitis can affect almost all organs, since blood vessels are everywhere. More often external signs diseases can be observed on:

• ears;
• oral cavity;
• paws;
• tail;
• stomach.

Signs and symptoms

Characteristic symptoms of the disease:

• pinpoint ulcers, especially common on the ears, lips, scrotum, tail, and oral mucosa;
• vascular lesions resemble bruises in appearance;
• skin necrosis in the form of spots, especially noticeable on the paw pads;
• sudden unexplained bleeding;
• swelling of the affected areas;
• fever;
• deterioration general condition(weight loss, poor appetite).

The dog has chronic arthritis and bursitis. But tests in most cases show the absence of these diseases.

On a note! The presence of other symptoms, as well as the absence of some of those listed above, does not guarantee the absence or presence of vasculitis. The manifestations of the disease largely depend on its cause. The presence of even some signs of vascular inflammation is a reason to immediately contact a specialist.

Diagnostics

Standard diagnosis of vasculitis includes:

• general blood and urine analysis;
• blood biochemistry;
• Ultrasound of the abdominal organs;
• X-ray;
• angiography;
• skin biopsy;
• allergy tests (if an allergic nature of the disease is suspected).

It is necessary to differentiate vascular inflammation from other diseases:

• pemphigus;
• drug dermatitis;
• cryoglobulinemia;
• ischemic necrosis;
• cold agglutinin syndrome.

Treatment methods

The main goal of vasculitis therapy is to eliminate the cause that caused the autoimmune reaction. But if the causes of inflammation remain unclear, it is required symptomatic therapy to alleviate the dog's condition. Depending on the severity clinical manifestations and the etiology of the disease, a whole range of medications is prescribed.

Trental

It is recommended to start therapy with Trental (Pentoxifylline). It is a derivative of methylxanthine. Trental increases the elasticity of blood vessels, makes the blood less viscous, and improves blood flow through swollen vessels. The product suppresses the production pro-inflammatory cytokines. Pentoxifylline is prescribed at a dosage of 15 mg/kg three times a day. A clinical response to the medication can be expected 1-3 months after the start of treatment.

Nonsteroidal immunosuppressants

These are drugs that are aimed at suppressing the immune system. Thus, the production of antibodies to one’s own cells is reduced.

Immunosuppressants include:

• Azathioprine;
• Chlorambucil;
• Leflunomide.

After achieving remission, the dose and frequency of medication is gradually reduced for long-term maintenance therapy. These drugs are recommended to be used in combination with corticosteroids.

Antibiotics

To prevent the development of secondary pyoderma against the background of vasculitis, prescribed systemic antibiotics prolonged action. Antibiotic therapy should be carried out simultaneously with a course of immunosuppressive drugs. This allows you to keep autoimmune processes in the body under control. A combination of antibiotics from the group of tetracyclines with niacin is effective for vasculitis.

Glucocorticosteroids (GCS)

Steroid therapy is effective for severe forms vasculitis in dogs. GCS allow you to quickly relieve inflammation, while also having an immunosuppressive effect. For several weeks, Prednisolone or Methylprednisolone is prescribed in combination with immunosuppressants. After removal acute manifestations diseases, the dosage of GCS is gradually reduced over 8-10 weeks.

If there is no significant improvement after 2-4 weeks, your doctor may prescribe alternative steroids:

• Dexamethasone,
• Triamcinolone.

Dogs, long time hosts hormonal drugs, must constantly undergo control of general and biochemical analysis blood.

Detoxification therapy

To speed up the elimination of toxins that accumulate in the body against the background inflammatory process, the dog is additionally prescribed sorbents:

• Atoxyl;
• Polyphepan;
• Enterosgel.

On the page you can find instructions for using the drug Hepatovet for dogs with liver diseases.

IN severe cases Infusion solutions are administered intravenously:

• glucose;
• Ringer solution;
• saline solution

Local therapy

To reduce local vascular inflammation and reduce doses systemic drugs, it is recommended to apply hormone-containing ointments or solutions to the affected skin. They are applied 2 times a day for no more than 3 weeks. They need to be abolished gradually. It must be remembered that local hormonal agents may cause side effects. Therefore, they must be used carefully.

Under no circumstances should you self-medicate. Therapy requires taking very strong medications, the improper use of which is very dangerous for the animal’s immunity and can cause irreversible changes in the body. If you suspect any problems with blood vessels, you should contact a specialist and carefully examine your pet.

Article from the book “A Color Handbook of Skin Diseases of the Dog and Cat” SECOND EDITION 2009 G

Translation from English: veterinarian Vasiliev AB

Etiology and clinical manifestations

Cutaneous vasculitis is inflammatory disease blood vessels, which is usually secondary to the deposition of immune complexes in the vessel walls. Vasculitis is usually associated with infections (bacterial, viral, fungal, rickettsial), malignant tumors, reactions to drugs, rabies vaccination, metabolic diseases ( diabetes, uremia), systemic lupus erythematosus or hypothermia (cold agglutinin disease) or may be idiopathic. It is uncommon in dogs and rare in cats.

In most cases, clinical symptoms characterized by purpura, necrosis and pinpoint ulcers, especially on the pinnae, lips, oral mucosa, finger pads, tail and scrotum. Acrocyanosis may occur. Vasculitis in the form of urticaria (acute onset of intense erythroderma with confluent erythematous wheals that do not blanch) has been described in dogs due to food hypersensitivity. In some dogs with rabies vaccine-induced alopecia, a focal area of ​​alopecia that develops at the site of vaccine administration appears 1 to 5 months after the appearance of multifocal lesions. skin lesions caused by generalized ischemic dermatopathy. These lesions are characterized by variable alopecia, crusting, erosions and ulcers in the margins of the ears, periocular areas, skin over bony prominences, tip of the tail and finger pads. Erosion and ulcers of the tongue may also be observed. Animals with cutaneous vasculitis may present with concurrent anorexia, depression, fever, arthropathy, myopathy, and pasty edema of the extremities.

With idiopathic vasculitis of the canine auricles, to which dachshunds are predisposed and dogs of other breeds are less likely to get sick, the affected animals first develop alopecia along the edges of the auricles. The skin in focal areas (0.2–2.0 cm) along the same edge of the auricle then becomes darkened, slightly thickened, and necrotic, leading to ulceration (Figure 22). Typically, both ears are involved and each will have one to eight lesions. Sometimes, small ulcers are not visible on internal parts auricle. The lesions do not appear painful or itchy and there are no other skin or systemic symptoms. If left untreated, the ulcers will slowly enlarge.

Differential diagnosis

For dogs with ear lesions only differential diagnosis should also include:

• Proliferative thrombovascular necrosis
• Disseminated intravascular coagulation
• Cold agglutinin disease
• Cryoglobulinemia
• Ischemic necrosis associated with intoxication

Diagnosis

1. Rule out other differential diagnoses.
2. Titers for rickettsial infections must be determined to exclude diseases caused by ticks.
3. Dermatohistopathology: neutrophilic, eosinophilic or lymphocytic vasculitis. In ischemic dermatopathy caused by rabies vaccination, cases of moderate to severe follicular atrophy, collagen hyalinization, and mural folliculitis may occur.

Treatment and prognosis

1. Any underlying disease must be identified and corrected.
2. To treat or prevent secondary pyoderma in dogs, appropriate long-acting systemic antibiotics (minimum 4 weeks) must be prescribed. Dogs treated with antibiotics during the induction phase of immunosuppressive therapy have significantly more high performance survival than dogs treated with immunosuppressive drugs alone. Antibiotic therapy should be continued as long as concurrent immunosuppressive drug therapy keeps the autoimmune disease under control.
3. The goal of treatment is to control the disease and its symptoms as much as possible. safe treatment, using the lowest possible doses. Ideally, drug combinations should be used to provide a comprehensive treatment plan to minimize side effects any one drug. Depending on the severity of the disease, more or less should be selected aggressive treatment. To achieve remission of the disease, higher doses are used initially and then reduced over 2-3 months to the lowest effective dose.

• Topical treatment, given every 12 hours in the form of steroid-containing drugs and tacrolimus, helps reduce focal inflammation and reduces the doses of systemic drugs required to control symptoms of the disease. Once remission occurs, the frequency of use should be minimized to reduce the incidence of local side effects.
• Conservative systemic treatment(see table) includes drugs that help reduce inflammation with minimal or no side effects. These drugs help reduce the need for more aggressive therapy, such as steroids or chemotherapy drugs. Steroid therapy is one of the most predictable treatments for autoimmune skin diseases; however, the side effects associated with the high doses required to control symptoms can be severe. Although glucocorticosteroid therapy alone may be effective in maintaining remission, the required doses may result in unwanted side effects, especially in dogs. For this reason, the use of non-steroidal immunosuppressive drugs, alone or in combination with glucocorticosteroids, is usually recommended for long-term maintenance treatment.
• Immunosuppressive doses of prednisone or methylprednisolone for oral administration should be prescribed daily (see table). Once the lesions have resolved (after approximately 2-8 weeks), the dose should be gradually reduced over a period of several (8-10) weeks to the lowest dose, possibly with alternate-day dosing, that maintains remission. If significant improvement is not observed within 2 to 4 weeks of initiation of therapy, concomitant skin infection should be excluded and alternative or additional immunosuppressive agents considered.
• Alternative steroids when prednisone and methylprednisolone are ineffective include triamcinolone and dexamethasone (see table).
• In cats, treatment with immunosuppressive doses of triamcinolone or dexamethasone is often more effective than therapy with prednisolone or methylprednisolone. Orally administered triamcinolone or dexamethasone should be given daily until remission is achieved (approximately 2-8 weeks), then the dose should be gradually reduced to the lowest possible dose with as little frequent use which supports remission (see table)
• If unacceptable side effects develop or there is no significant improvement in the first 2-4 weeks of treatment, consider the use of alternative corticosteroids or non-steroidal immunosuppressive drugs (see table).

• Alternative treatments that may be effective include the following:
• Dapsone (dogs only) 1 mg/kg PO every 8 hours until lesions resolve (approximately 2-3 weeks). Once remission is achieved, the dose is gradually reduced to 1 mg/kg PO every 12 hours for 2 weeks, then 1 mg/kg every 24 hours for 2 weeks, then 1 mg/kg every 48 hours.
• Sulfasalazine 10–20 mg/kg (maximum 3 g/day) orally every 8 hours until lesions resolve (approximately 2–4 weeks). Once remission is achieved, the dose is reduced to 10 mg/kg every 12 hours for 3 weeks, then 10 mg/kg orally every 24 hours.
• Nonsteroidal immunosuppressive drugs that may be effective include azathioprine (dogs only), chlorambucil, cyclophosphamide, mycophenolate mofetil, and leflunomide (see table). A positive response is observed within 8-12 weeks from the start of therapy. Once remission is achieved, attempts are made to gradually reduce the dose and frequency of nonsteroidal immunosuppressive drugs for long-term maintenance treatment.

4 Regardless of the drug used, therapy may eventually be discontinued in some patients after 4 to 6 months of treatment; in others, long-term maintenance therapy is necessary to maintain remission.

5 The prognosis is variable, depending on the underlying cause of the disease, the extent of skin lesions, and the degree of involvement of other organs.

Photo 1 Vasculitis of the skin of dogs and cats.

Photo 2 Vasculitis of the skin of dogs and cats. Erythematous lesions with alopecia on the face of an adult Jack Russell Terrier

Photo 3 Vasculitis of the skin of dogs and cats. The same dog from photo 2. Erosive lesions on the hard palate are typical for vasculitis. Lesions of the oral mucosa are often observed with vasculitis, pemphigus vulgaris, bullous pemphigoid and systemic lupus erythematous (SLE).

Photo 4 Vasculitis of the skin of dogs and cats. Alopecia, crusts on the edge of the auricle are typical for vasculitis. Note the similarity to scabies; however, the dog did not experience intense itching.

Photo 5 Vasculitis of the skin of dogs and cats. Multiple defects in the form of indentations on the edge of the auricle in adult dachshund. There is no obvious inflammation, which is an indicator of active vasculitis.

Photo 6 Vasculitis of the skin of dogs and cats. Large defect in the form of perforation caused by chronic vasculitis of the auricle

Photo 7 Vasculitis of the skin of dogs and cats. Peripheral edema caused by leakage of fluid from blood vessels due to vasculitis.

Photo 8 Vasculitis of the skin of dogs and cats. An erythematous lesion with well-defined snake-like edges is characteristic of vasculitis, a skin reaction to drugs (erythema multiforme), or an autoimmune skin disease.

Photo 9 Vasculitis of the skin of dogs and cats. Severe ulcerative dermatitis on the paw of an adult greyhound. Note the well-circumscribed snake-like edges of the lesion, which is characteristic of vasculitis, a skin reaction to drugs (erythema multiforme), or an autoimmune skin disease.

Photo 10 Vasculitis of the skin of dogs and cats. Focal ulcerative lesion in the center of the pad is unique feature vascular disease.

Photo 11 Vasculitis of the skin of dogs and cats. Cortical lesions on the pads (especially the central ones) are a unique feature of vasculitis.

Photo 12 Vasculitis of the skin of dogs and cats. Peeling of the skin of the toe pads in a dog with vasculitis. Damage to the fingertips may also occur with autoimmune skin diseases.

Photo 21 Vasculitis of the skin of dogs and cats. Pad ulcers in a dog with vasculitis.

Photo 22 Vasculitis of the skin of dogs and cats. Alopecia, crusts on auricle. The nasal planum is not changed. Note the similarity of the lesions to scabies; In this dog, the itching was mild.

Text of the article and photos 1-21 from the book

SMALL ANIMAL

DERMATOLOGY

A COLOR ATLAS AND THERAPEUTIC GUIDE

Paul B. Bloom 1"2

1. Clinic for Allergy, Skin and Ear Diseases of Pets, Livonia, USA
2. Faculty clinical veterinary medicine Small Animals, Department of Dermatology, University of Michigan State University, USA

Editor's note. The presented classification of vasculitis does not correspond to that accepted in domestic medicine. In our practice, vasculitis is divided into primary and secondary and classified depending on clinical signs, the size of the affected vessels and the type of cellular infiltrates. Vasculitis and vasopathy are generally considered synonymous.

Review

Ischemic skin lesions can be divided into two groups: forms with abundant cellular infiltrate (vasculitis) and poor cells (vasopathy). Regardless of the form, they are all associated with inadequate microcirculation in the skin.

Vasculitis is characterized by an aberrant immune response aimed at blood vessels. Histologically, there is an inflammatory response involving and destroying blood vessels, leading to ischemic changes (see histology). Vasopathy (small cell vasculitis) is also pathological process, in which they take place ischemic changes tissue, but histologically there is a small number inflammatory cells. Differentiation between vasculitis and vasopathy is not important for the treatment of patients suffering from this condition.

Clinically, vasculitis may present as either a purely cutaneous form or a systemic form (eg, uveitis, glomerulonephritis) or both ( mixed form). Vasculitis can be caused by drugs (including vaccines), bacterial, viral, fungal or rickettsial infection (both direct exposure to the pathogen and as a result of the formation of immune complexes (type III hypersensitivity reaction)), idiopathic/genetic causes (jack- Russell Terriers), neoplasms, skin reactions for food or autoimmune disease(systemic lupus erythematosus, SLE).
Cutaneous small vessel vasculitis (SVVV) affects small vessels dermis, especially postcapillary venules. KVMS is the most common form cutaneous vasculitis dogs. The most commonly used method to classify vasculitis in dogs is the assessment of skin infiltration. There are neutrophilic leukocytoclastic, neutrophilic non-leukocytoclastic, lymphocytic, eosinophilic and granulomatous forms. It is important to realize that the result of a biopsy depends on the time the sample is taken. The predominant cell type in a biopsy may simply reflect the specific stage of the disease, rather than its type. For leukocytoclastic CVMS, if the biopsy was performed early (<24 часов от начала заболевания), можно увидеть гранулоцитарный инфильтрат, а при биопсии спустя 48 часов или позже он будет в основном лимфоцитарным. Встречаются и формы КВМС с изначально лимфоцитарной картиной (напр., вакциноассоциированный).

Clinical manifestations of CVMS

Clinical signs of CVMS include scaling, hair loss, purpura (palpable papules and nodules with a hemorrhagic component), ulcers, blisters, nodules, congestive edema, acrocyanosis, and panniculitis (if deeper vessels are involved). The elements are located on the distal parts of the limbs (including the tips of the ears and tail) and pressure points. Systemic lesions may be observed as a consequence of vasculitis (liver damage, glomerulonephritis, synovitis/arthritis, gastroenteritis, pleurisy/pericarditis) and/or underlying disease (eg, anemia and/or thrombocytopenia in SLE).
A number of vasculitides have been described. The etiology of some is known, for others it is unclear. These include:

1. Urticarial vasculitis, which is a special subtype of CVMS. The clinical picture is represented by blisters or serpentine papules, sometimes with nearby or distantly localized angioedema. Unlike other forms of urticaria, urticarial vasculitis resolves slowly, often over several days, and may be accompanied by purpura. This form is often associated with food intolerance.
2. Proliferative thrombovascular necrosis of the auricle has an unclear etiology. This disease has no connection with gender/breed/age. The elements appear at the tip of the ear and extend proximally to the inner surface. The elements are wedge-shaped, with the tip of the wedge located proximally. Ulcers, crusts and peeling are observed.
3. A familial (autosomal recessive) cutaneous vasopathy of German shepherd dogs has been described in Canada. This genodermatosis is often caused by vaccination: elements appear 7-10 days after vaccination. The puppy shows signs of systemic damage (drowsiness, lameness, swelling in the joints, fever +/lymphadenopathy). Skin manifestations include tight swelling of the bridge of the nose, ulcers and crusts on the auricle, nose and tip of the tail. The paw pads are swollen, depigmented and may ulcerate. General and biochemical blood tests, ANA titers, RF, Coombs reaction and immunoglobulin levels are within normal limits.

1. Proliferative arteritis of the nasal lobe has been described in St. Bernards and Giant Schnauzers. The author also made the same diagnosis for the Great Dane. Etiology unknown. There are non-pruritic linear ulcers on the nose, sometimes with severe bleeding. In the treatment of this disease, success is unpredictable. Prednisolone, topical hormonal drugs, tetracycline, niacinamide and fatty acids (omega-3/omega-6 combination) are used.
2. Idiopathic cutaneous and glomerular vasopathy in racing greyhounds (“Alabama rot”). There is no connection with gender or age. There may be a genetic predisposition to this disease. Clinically, it begins with multifocal erythematous swelling of the skin, which later ulcerates. Elements are noted on the limbs +/ abdomen and torso. Serous-hemorrhagic discharge may leak from the elements. Pastosity may be observed. Systemic lesions have been described (fever, drowsiness, gastrointestinal involvement), including symptoms of acute renal failure. The etiological factor is considered to be verotoxin produced by E. coli found in undercooked beef products.
3. Scottish terrier vasculitis has been described as a probable genodermatosis. At 3-4 weeks of life, dogs begin to have discharge from the nose, followed by ulceration and destruction of the nose and nostrils. There is no effective treatment.
4. Vasculitis has been described in Jack Russell Terriers. In one description, the dogs' ages (5) ranged from 3 months to 11 years. The cause of the disease is unknown, but 3 out of 5 dogs developed symptoms 2-3 weeks after vaccination. The author believes that these dogs may have had a late onset of dermatomyositis. There is a high probability that they had vasculitis.
5. Familial canine dermatomyositis is an ischemic skin and/or muscle disease with a genetic basis (collie and sheltie). This is the only ischemic skin lesion that is accompanied by muscle involvement. The age of debut is from 6 weeks to 1 year, usually up to 6 months. The elements may decrease and disappear as you grow older, or they may progress. Usually the elements disappear by 1 year of life. Skin lesions that are usually the most prominent clinical sign include alopecia, desquamation, crusting, erosions, ulcers, depigmentation, hyperpigmentation, and scarring. Elements appear on the muzzle, mucocutaneous junctions, metacarpus and metatarsals, at the tips of the tail and ears. Onychodystrophy may also occur. Secondary bacterial pyoderma may occur. Muscle involvement is proportional to the severity of the skin lesions and is usually detected after the skin lesions have developed. These dogs may develop megaesophagus, or muscle wasting, involving the masseter and extensor muscles. The differential range includes demodicosis, dermatophytosis, superficial bacterial folliculitis, discoid lupus erythematosus and epidermolysis bullosa. In the author's experience, most often puppies have limited damage to the muzzle, which the owner mistakes for wounds/scars received from other puppies or cats in the house. Diagnosis is based on the dog's characteristics, physical examination, and histologic changes consistent with vasopathy.

1. Idiopathic CMS can occur in dogs of any breed or age. This diagnosis is made after excluding genetic predisposition and all other possible causes.
2. Post-vaccination alopecia after rabies vaccination is an ischemic skin lesion that occurs 2-12 months after administration of the rabies vaccine. The risk group includes small breed dogs with white fur. The method of vaccine administration does not affect the incidence of this reaction. Skin lesions include scaling, hair loss, plaques, hyperpigmentation, nodules, erosions, crusts, and skin atrophy (scar formation). Elements can also occur far from the site of vaccine administration. Histologically, in addition to the changes characteristic of vasculitis, septal panniculitis and focal lymphoid nodules can be observed.

Pathophysiology of CVMS

Regardless of the causative/trigger factor that provokes the development of vasculitis, an immunological hypersensitivity reaction is triggered. This reaction leads to vascular damage and ischemic changes that are observed clinically. Hypersensitivity reactions include the following.

1. Type I occurs when 2 IgE molecules on the surface of mast cells bind antigen, resulting in degranulation of mast cells and the release of both stored and newly synthesized mediators, which include histamine, leukotrienes, chemokines and cytokines. Chemokines and cytokines mobilize leukocytes, including eosinophils, NK cells and T lymphocytes. This type of hypersensitivity is most often associated with insect bites, but can also occur in response to food components. Histological examination reveals a pronounced eosinophilic infiltrate.
2. Type II involves antibodies of the IgM and IgG classes, landing on circulating cells or directly on tissue antigens - in this case, endothelial ones. Attachment of these antibodies to the surface of these cells (opsonization) allows phagocytes to attach. Once bound, the phagocytes release the contents of their lysosomes, resulting in endothelial cell death. Antigen-antibody binding can also activate the complement system. When activated, the complement system leads to lysis and death of endothelial cells. Finally, antibodies can bind to NK cells (cytotoxic lymphocytes). After binding to the endothelial cell-antibody complex, these cells activate enzymes leading to apoptosis (cell death).
3. Type III occurs when there is a supply of soluble antigen-antibody complexes (IgG or IgM) that are normally cleared by macrophages in the spleen or liver. These complexes can be deposited on or between endothelial cells. When this happens, the complement system is reactivated, leading to cell death.
4. Type IV hypersensitivity reaction is associated with an abnormal response of T lymphocytes to antigen. Once sensitized by antigens, these T lymphocytes infect tissues. Cytotoxic CD8+ T lymphocytes cause direct damage, while T helper 1 (CD4) cells secrete cytokines that activate cytotoxic T lymphocytes and mobilize and activate macrophages. Activated macrophages produce inflammatory cytokines, which are a major cause of cell damage.

It is important to understand that the immune system reacts abnormally to an antigen, involving various mechanisms. If we can detect this antigen, treatment is more likely to be successful.

Differential diagnosis

Vasculitis is differentiated from coagulopathies, cold agglutinin disease, frostbite, DIC syndrome, demodicosis, dermatophytosis, superficial bacterial folliculitis and discoid lupus erythematosus.

Diagnostics

Diagnosis of any skin disease is based on a thorough history, clinical manifestations (primary localization, nature and distribution of elements), laboratory tests and response to treatment. The most valuable laboratory technique for vasculitis is histological examination. Evaluation of patients with confirmed vasculitis should include a detailed medication history (including vaccinations), a thorough physical examination (including retinal examination), and basic laboratory testing such as complete blood count, chemistry panel, and urinalysis. To detect nephropathy accompanied by protein loss, the total protein/creatinine ratio should be determined or a microalbuminuria test should be performed. Other diagnostic procedures depend on the dog's characteristics and clinical picture. These include identifying mites, culture of blood, tissue or urine samples, Coombs test, determination of ANA (antinuclear antibodies), X-ray of the chest and abdomen, ultrasound of the abdominal organs.

Histology

Because the number of histological manifestations of vasculitis is limited, it makes sense to think of vasculitis as a pattern of response to a number of different etiological factors. Regardless of the cause, vasculitis is a pathological process characterized histologically by inflammation and destruction of blood vessels, as well as ischemic changes manifested by blurring and pallor of skin collagen, scant cell superficial dermatitis, dyskeratosis of keratinocytes, necrosis of the entire thickness of the epidermis, atrophy of follicles and skin appendages and folliculitis .

Treatment

The first step is to identify and treat the causative condition (if possible) and/or avoid it (eg, if there is a reaction to medications). After determining a treatment plan, you should make sure that the treatment will not cause more harm than the disease itself. Depending on the severity of symptoms, treatment may include: pentoxifylline, glucocorticosteroids (GCS), other immunosuppressants, cyclosporine and immunomodulators.

In any case, if systemic treatment is necessary, the author starts with pentoxifylline (Trental), both alone and in combination with other drugs. Pentoxifylline is a methylxanthine derivative that increases the elasticity of red blood cells and reduces blood viscosity, improving blood flow through narrowed/edematous vessels. It also inhibits the synthesis of pro-inflammatory cytokines such as IL-1, IL-4, IL-12 and TNF-. Pentoxifylline is prescribed at a dose of 15 mg/kg 3 times a day. Complete clinical response may be achieved with a delay of 30-90 days.

Vitamin E (400-800 IU 2 times a day) and essential fatty acids (omega-3) are prescribed for their anti-inflammatory and antioxidant properties.

If systemic treatment is necessary, a combination of tetracycline and niacinamide can be added to therapy. This combination has many anti-inflammatory and immunomodulatory properties. The dosage of tetracycline and niacinamide for cats and dogs less than 10 kg is 250 mg of both every 8 hours, for dogs heavier than 10 kg - 500 mg of both every 8 hours. With a clinical response (which usually takes several months), the drugs are slowly withdrawn - first to 2, and then to 1 dose per day. Side effects are rare, but when they occur, they are usually caused by niacinamide. These include vomiting, anorexia, drowsiness, diarrhea, and elevated liver enzymes.

The basis of treatment for many forms of vasculitis are glucocorticosteroids (GCS). The most powerful veterinary local drug is synotic, containing fluocinolone acetonide. If the disease is localized (for example, at the tip of the ear), but cannot be treated with synotic, the author uses an even more powerful remedy - deoxymethasone at a concentration of 0.25%. These external preparations are applied 2 times a day. until clinical remission is achieved (but not more than 21 days), and then slowly withdrawn over several months. Make sure the owner wears gloves when applying this medication. Remember that local hormonal drugs can cause polyuria/polydipsia/polyphagia. This reaction to GCS is highly variable and can occur in unexpected situations. If side effects occur or there is no response to treatment, topical tacrolimus (0.1%) can be tried.

If more aggressive therapy is necessary, tetracycline/niacinamide is replaced with prednisolone, which is prescribed at a dose of 1 mg/kg twice a day. for 4 days, and then mg/kg 2 times a day. for the next 10 days. Repeated examinations are carried out every 14 days. If remission is achieved, the dose is reduced by 25% every 14 days. The author defines remission as the absence of active (fresh) elements. Do not reduce the dose too quickly! The goal is to keep the dog on 0.25 mg/kg or less every other day. If this is not possible, azathioprine is added to therapy (see below).

If the animal does not respond to prednisolone, then it is necessary not only to add other immunosuppressants (see below), but also to replace it with dexamethasone or triamcinolone. For both drugs, the initial dose is 0.05-0.1 mg/kg 2 times a day. Withdrawal occurs as gradually as with prednisolone.

Animals receiving GCS for a long time, regardless of the dose, require monitoring of general and biochemical blood tests, general urinalysis and urine culture (to exclude asymptomatic bacteriuria) every 6 months.

Azathioprine is an antimetabolite that is converted to its active form, 6-mercaptopurine, in the liver. 6-MP disrupts normal DNA and RNA synthesis, preventing cell division, leading to cell death. It is metabolized in the liver by 3 different enzyme systems, one of which is xanthine oxidase (XO). KO metabolizes azathioprine to an inactive metabolite. It should be remembered that allopurinol, which is a CO inhibitor, is used to treat urolithiasis in dogs. Do not administer azathioprine to dogs receiving allopurinol.

The effect of azathioprine reaches its full effect with a delay of 4-6 weeks. The drug is prescribed simultaneously with GCS. The initial dose of azathioprine is 1.0 mg/kg once a day. After achieving remission and discontinuation or reduction of corticosteroids to minimal doses, azathioprine intake is reduced every 2-3 months. The author usually reduces not the dose, but the frequency of administration, first prescribing every other day, and then once every 72 hours. Complete (with platelet count) and biochemical blood tests are monitored every 14 days for 2 months, then every 30 days for 2 months, then every 3 months for the entire period while the dog is on azathioprine. Possible side effects include anemia, leukopenia, thrombocytopenia, hypersensitivity reactions (especially in the liver) and pancreatitis. Azathioprine should not be given to cats as it may cause irreversible bone marrow suppression.

Chlorambucil is indicated for dogs that do not respond to or cannot tolerate azathioprine. The treatment regimen/precautions/monitoring for chlorambucil is the same as for azathioprine. Initial
dose 0.1-0.2 mg/kg/day.

In the case of neutrophilic vasculitis that does not respond to the treatment described above, sulfasalazine at a dose of 25 mg/kg 3 times a day may be effective. (maximum 3 g per day). Side effects include anemia, keratoconjunctivitis sicca and hepatotoxicity, so it is necessary to monitor general and biochemical blood tests and the Schirmer tear test every 14 days for 2 months, then every 30 days for 2 months, then every 3 months for the entire period while the dog is sulfasalazine. If neutrophilic vasculitis does not respond to sulfasalazine, dapsone can be tried, although it is more toxic than sulfasalazine.

For eosinophilic or urticarial vasculitis, or any vasculitis that does not respond well to treatment, the dog should be placed on a homemade elimination diet.

Bibliography

1. Scott DW, Miller WH, Griffin CE. Muller & Kirk's Small Animal Dermatology. 6th ed. Philadelphia: WB Saunders; 2001:742-56.
2. Nichols PR, Morris DO, Beale KM. A Retrospective Study of Canine and Feline Cu-taneous Vasculitis. Vet Dermatol 2001: 12:255-264
3. Affolter VK. Cutaneous Vasculitis and Vasculopathy. In: World Small Animal Veterinary Association World Congress Proceedings, 2004
4. Torres SM, Brien TO, Scott DW. Dermal arteritis of the nasal philtrum in a Giant Schnauzer and three Saint Bernard dogs. : Vet Dermatol. 2002: 13:275-81.
5. Hargis AM, Mundell A. Familial canine dermatomyositis. Comp Cont Ed Pract Vet 1992; 14:855-65.
6. Rees CA, Boothe DM. Therapeutic Response to Pentoxifylline and Its Active Me-tabolites in Dogs with Family Canine DermatomyositisVet Ther 2003:4:234-241
7. Vitale CB et al. Vaccine induced ischemic dermatopathy in the dog. Vet Dermatol. 1999; 10:131.
8. White SD, Rosychuk RAW, Reinke SI, et al. Tetracycline and niacinamide for treatment of autoimmune skin disease in 31 dogs. J Am Vet Med Assoc 1992:200:1497-1500.

Prepared based on materials: “PROCEDINGS OF THE MOSCOW INTERNATIONAL VETERINARY CONGRESS, 2012.”