Demodicosis in dogs: ways of infection and drugs for the treatment of the disease. This insidious and dangerous demodicosis in dogs: what breeders need to know

Demodicosis in dogs can be caused not only by a weakened innate immune system. Other factors also influence the appearance of the disease:

• hormonal disruptions;
• malnutrition;
• oncological diseases;
• medicines that cause immunodeficiency (hormonal drugs, chemotherapy).

As a rule, adults suffer from demodicosis. Up to a year of life in an animal, only juvenile demodicosis can manifest itself, which, as it grows older, disappears on its own. In most cases, it is caused by the fact that the dog's immunity has not yet been fully developed.

The development of the disease most often begins in the autumn or spring.

Classification and symptoms of demodicosis

There are several types of skin disease:

• focal;
• juvenile;
• generalized.

Focal demodicosis is considered the safest. The disease manifests itself in small affected areas in 3-5 places. On infected integuments, the skin is flaky and has no hair. Locations are:

• head;
• breast;
• stomach;
• paws.

If the animal does not have any other diseases, then in about 80 out of 100 cases, a self-healing occurs. The danger of the focal form is that if it is not treated, then there is a high probability of relapse. For treatment, topical preparations are used. Sometimes focal demodicosis can go into a generalized form.

Generalized demodicosis in dogs, symptoms:

• damage to large areas of woolen integument;
• in more severe cases, damage to internal organs occurs;
• bald areas become gray or red, emitting an unpleasant odor.

Puppies and young dogs up to 1 year old are predisposed to the juvenile form. A sign of the disease is the formation of bald areas in the paws, as well as around the eyes in the form of "glasses". In rare cases, juvenile demodicosis acquires other more severe forms.

Important! Treatment of demodicosis in dogs must be present, regardless of the form of the disease.

Differentiation of demodicosis from other diseases

Demodicosis should not be confused with diseases such as:

• otodecosis;
• sarcoptic mange;
• notoedrosis;
• microsporia;
• alimentary dystrophy;
• infectious diseases.

Otodectosis is an ear scabies and, as a rule, it is not difficult to distinguish it from demodicosis. The place of localization of the disease is exclusively the auricles, the defeat of which occurs inside and outside the ear, due to the fact that the dog begins to intensively comb itchy places. When otodectosis, the ears are affected by mites of the species Otodectes cynotis.

Notoedrosis is caused by causative agents of head scabies of carnivorous Notoedres cati. The disease is characteristic of young individuals. First of all, ticks of this species affect the integuments of wool and skin on the head. Numerous papules and vesicles appear. The skin becomes folded and crusty in the affected areas.

Microsporia and trichophytosis is a ringworm. The causative agents are fungi of the genus Trichophiton et Microsporum. Symptoms of ringworm are severe itching and hair fragments in the affected areas, peeling of the epithelium and swelling. In areas of localization, it seems that the hairs are cut off.

Alimentary dystrophy occurs as a result of an inadequate and unbalanced diet. The disease is characterized by such a main symptom as constant molting. In this case, itching is not observed.

For such infectious diseases as necrobacteriosis, pasteurellosis, damage to the skin and wool is characteristic. In addition, there is fever, exhaustion, dysfunction of internal organs. These symptoms are caused by viruses and bacteria.

First aid for demodicosis

When the first signs of the disease are detected, the affected parts of the skin are smeared with fish oil and the bedding where the dog sleeps is changed as often as possible. The animal should be taken to the hospital as soon as possible.

After examination by a doctor, the necessary therapy and tests are prescribed. The first thing you need is to bathe your pet with an antibacterial shampoo and apply a special antiseptic lotion.

Medications are prescribed by a doctor depending on the form of the disease and the breed of the dog. In addition, the animal is put on a diet that should include vitamin A and E.

Treatment regimen for demodicosis in dogs

For any form of the disease, the drug "Gamavit" is recommended for use, which is an antioxidant, adaptogen, detoxifier and normalizer of the blood formula. In addition, it reduces the toxicity of acaricidal agents. The drug is used in combination with the Gamabiol balm, which eliminates the inflammatory processes of the skin.

Focal and juvenile demodicosis

In the case of a focal form, first of all, it will be necessary to ensure that the disease does not develop into a generalized one.

The focal form is recommended to be treated with local preparations. The remedy can be prepared independently from equal parts of solar oil, carbon tetrachloride and turpentine. In addition, a 1% trypansini solution is used subcutaneously or intravenously. In combination with the solution, sedimentary sulfur powder is used as a local agent.

Effective local remedies in the treatment of focal form are:

• 5% soap emulsion;
• 1% sevin emulsion;
• 2% solution of chlorophos;
• 1% coral emulsion;
• 2% emulsion SK-9.

At the same time, chlorophos is used for oral administration at a dosage of 25 mg per 1 kg of body weight.

In addition, antibacterial drugs are prescribed for home treatment, which are taken from 1 to 3 months, depending on the severity of the disease. Taking antibiotics reduces the risk of a secondary bacterial infection. To eliminate ticks, drugs such as Milbemycin and Ivermectin are prescribed.

Attention! Ivermectin is contraindicated for dogs of the Australian Shepherd, Collie and Sheltie breed. Drugs in this group can lead to serious side effects, even death.

Other breeds are less sensitive to the drug, so the manifestation of side effects is extremely rare.

When carrying out treatment, it is important to regularly bathe the dog with antiseptic agents - this will help your pet recover faster.

In the juvenile form, the animal, in addition to the above remedies, is prescribed vitamin E, which stimulates tissue regeneration.

Generalized demodicosis

The most complex form of the disease, like generalized demodicosis, requires complex therapy.

It should be remembered that none of the drugs for generalized demodicosis does not guarantee a 100% cure.

For home treatment, the following drugs are prescribed:

• antimicrobial;
• antifungal;
• antitoxic;
• adaptive;
• immunomodulating;
• acaricidal.

Acaricides include:

• Dectomax;
• Milbemycin;
• Ivomek;
• Seifli;
• based on amitraz.

Immunomodulatory drugs:

• Maksidin;
• Fosprenil.

The dog should be treated under regular medical supervision. The course of treatment can last from 3 months to six months, and sometimes more. During this period, after one to two weeks, it is necessary to undergo laboratory tests. A skin scraping is performed and its further microscopy, which makes it possible to determine the effectiveness of the prescribed therapy.

Important! Do not self-medicate your dog. Incorrectly prescribed treatment can lead to complications and death of the animal.

Diet

With demodicosis, the dog should receive food rich in vitamins A and E. A protein-restricted diet is used, the consumption of which should be reduced by 2-3 times.

Prevention

Preventive measures will help prevent relapse, which include:

1. Hygiene. Change the bedding on which the animal sleeps as often as possible. Groom your coat and use specialized bath shampoos.
2. Complete nutrition. The pet should receive a balanced diet that helps maintain the immune system and health.
3. Preventive checkup. Every three months the dog must be shown to the veterinarian.

During the natural shedding process, some doctors recommend adding sulfur to your pet's diet.

Dogs suffering from decomedosis are castrated and sterilized, as there is a high probability of transmitting the disease to offspring.

Forecast

In most cases, it is not possible to completely get rid of demodicosis, but stable remission can be achieved. Depending on the form of the disease, treatment can last from several months to several years. Proper selection of drugs and an integrated approach to treatment increase the chances of recovery. Dogs younger than 3 years of age respond better to treatment than older animals.

In contact with

This parasitic disease, caused by a certain genus of mites (Demodex canis), most often affects young animals and over the age of 10 years. The danger and insidiousness of the disease lies in the fact that in the initial stages the infection practically does not manifest itself, but not only the skin, but also the internal organs can gradually be affected. Demodicosis often causes the death of dogs. How to protect your pet and what to do if a terrible diagnosis is confirmed - find out with us soon.

What is demodicosis or red scabies?

Demodicosis in dogs is often referred to as red scabies. This name is quite understandable if you look at a photo or a real picture of the manifestation of the disease. However, the dog owner should remember that the disease is not contagious to other animals or humans. A person can get demodicosis, but clinical studies show that its causative agent is not a canine or feline species of ticks.

Recently, you can find information that demodexes (mites) are part of the normal flora of dogs. And some breeds generally manifest a hereditary ailment (boxer, rottweiler, bulldog and other short-haired breeds). However, this issue is controversial, as evidenced by numerous studies of veterinarians. Even if absolutely healthy pets have ticks, this cannot be considered a normal phenomenon.

Demodex mites under the microscope

Symptoms

It is easy to recognize demodicosis in dogs, the symptoms of which manifest themselves in the form of a specific skin lesion, as in the photo below. At the initial stage, the animal may itch, red spots appear at the base of the hair. After another time, usually 2-3 days, small blisters with reddish-clay contents appear at the site of redness. When the blisters burst, hair falls out on the affected areas. Demodex is located in the hair follicles - as a result of this, hair loss occurs.

Often a slightly different picture can be observed. On the affected areas, dry scales appear on the skin, which stick together the hair. After a while, the scales fall off, and pus appears on the skin under them. In addition, the disease is accompanied by general oppression of the animal, the dog may refuse food, be lethargic. Body temperature drops to 37 degrees.

Diagram of tick distribution in dogs

However, there are two points of view on the way of infecting pets with ticks. The first, which says that demodexes are part of the normal flora of a dog, considers a decrease in immunity, as well as hormonal disruptions, to be the main cause of the development of the disease. Another point of view, which denies the presence of ticks in the normal flora of a dog, says that the main route of infection is already sick individuals. In addition, puppies during the lactation period are at risk - ticks are transmitted from the mother.

The reasons for the development of demodicosis can be called:

• lack of vitamins and proteins - improper feeding;
• worm infection;
• stress and other negative external factors of content;
• transferred viral and infectious diseases;
• prolonged use of antibiotics;
• rickets;
• general immunodeficiency;
• heavy loads;
• genetic susceptibility of dogs.

Treatment Methods

Demodicosis is a complex disease, so it is best to treat a dog under the strict supervision of a veterinarian. When the first symptoms are detected, drugs are prescribed to kill the tick (drops, ointment) along with general therapy for restoring immunity, removing toxins from the body, and treating the skin. If the disease is advanced and the specialist diagnoses a generalized form of demodicosis, then several directions of therapy are used at once. Namely: antimicrobial and antifungal, antitoxic, immunomodulatory and immunoprotective, treatment or maintenance of internal organs (liver, kidneys, heart).

Treatment of demodicosis is always complex, in addition to the drug from the tick, an immunostimulant is used and, if necessary, means to combat the secondary microflora. With strictly localized single foci in young dogs, many veterinarians do not use treatment, since the disease will go away on its own when immunity is strengthened.

As for the destruction of the tick itself, the therapy is carried out in two ways and is associated with the form of the disease. Against adults, special ointments are used, for example, Aversectin ointment, as well as complex preparations such as Bravecto. If ticks are near blood vessels, then treatment is carried out with the help of drugs Ivermectin and Doramectin. When treating the skin, a special analysis of bakposev is necessarily carried out first, the type of microbes and their sensitivity to antibiotics are determined. Then, based on the analysis, a drug or ointment is prescribed.

We offer you to learn more about all the features of the Bravecto drug from the video webinar about demodicosis. What is the effectiveness of Bravecto, a representative of the manufacturer's company will tell (video from Uralbiovet-Consulting).

Folk remedies

As for the treatment of folk remedies, they are applicable only for the scaly form of demodicosis. So, for example, decoctions of St. John's wort, wormwood, ointment based on celandine give a positive result. To kill ticks, you can find tips on using tar soap and any available acaricides. For the speedy recovery of the skin from folk remedies, you can use milk thistle, flax and vitamin E. Gamavit is also applicable at home (not as a remedy for demodicosis, it is more of an immunostimulating drug), Bravecto, external agents (Lawyer - drops against ticks and others).

In addition to proper treatment, demodicosis requires a dog owner to correct nutrition, regulate stress and improve general conditions at home. To maintain the gastrointestinal tract during the treatment of demodicosis, probiotics and prebiotics are prescribed, as well as hepatoprotectors and general courses of vitamin and mineral supplements.

Video "Veterinary speaking"

In this video, you will hear an opinion on the treatment and features of demodicosis in dogs from a specialist in a modern veterinary clinic (video from Svoy Doktor Veterinary Clinic).

Demodicosis is one of the most common tick-borne diseases in dogs. Most often, German Shepherds, Rottweilers, Cocker Spaniels, Boxers, French Bulldogs, Dobermans, Great Danes and Dachshunds get sick.

The critical age is 1-2 years, and in puppies the disease is detected starting as early as 3 weeks (8). A person is also sick with demodicosis, however, reliable cases of isolation of dog or cat species of ticks from him have not yet been described.

For example, the fact of carriage of this tick in a number of short-haired breeds of dogs (Rottweiler, Boxer, Staffordshire Terrier, Bulldog) is well known, so the detection of D. canis in a dog is not yet a signal of invasion.

Demodicosis has a certain seasonality: Most often, clinical signs appear in the period from May to September. This is due to the fact that in warm weather, the already short tick development cycle is halved and is about 2 weeks. This feature determines the complexity of the struggle in the summer, since the female manages to lay many eggs in a short time.

The development of demodicosis is often promoted by improper feeding.(especially with regard to protein and vitamins), past infectious diseases, helminthic invasion, severe stress, rickets, cosmetic surgery, immunosuppressive (chemo- and glucocorticoid) therapy or long-term antibiotic treatment. Usually, the invasion develops against the background of immunodeficiency, often congenital. Among the primary immunodeficiencies, against which demodicosis occurs, one can single out IgA deficiency, as well as hereditary deficiency of immunity mediated by T-lymphocytes, the prognosis in such cases varies from cautious to unfavorable. The genetic susceptibility of dogs, predisposing to the development of this invasion, is manifested in the inability to develop delayed-type hypersensitivity in response to intradermal injection of Demodex antigens.

Many studies have shown that immunity suffers with demodicosis, erythrocytopenia, leukocytosis, lymphocytopenia, and monocytosis develop (6, 8).

Pathology is almost always accompanied by secondary microbial and fungal infections, sometimes by other invasions. These complications, as a rule, aggravate the course of the disease, intoxication, provoke dysbacteriosis, which is reflected in the biochemical and clinical parameters. Thus, in severe demodicosis, when mites can be found in the intestinal walls, liver parenchyma cells and other internal organs, there is a significant increase in total bilirubin, an average of 5-7 times (6).

Depending on the course of the disease, three main forms of demodicosis are traditionally distinguished:
- scaly (lighter),
- pustular
- generalized.

In a severe form of secondary fungal or bacterial (most often staphylococcal) infection and a generalized nature, sepsis can develop, which is fatal for the animal, treatment in these extremely rare cases is extremely difficult.

Obviously, the versatility of the forms of the course and the complex nature of the development of the disease require the creation of a whole range of therapeutic measures: it should include both specific therapy based on the use of acaricidal drugs and systemic maintenance therapy with the indispensable inclusion of modern immunostimulants. Since the generalized form of demodicosis is not a local, but a general disease of the whole organism, therapy should include antimicrobial, antifungal, antitoxic, adaptive, immunoprotective and immunomodulatory approaches (6).

Of the acaricides, preparations based on amitraz are often prescribed, as well as ivermectin (ivomec), milbemycin, tiguvon (contains fenthion - 0.0-dimethyl-0-(3-methyl-4-methylthiophenyl)-thiophosphate), an oral preparation " Sayfly "(contains cythioate - O-(4-amidosulfonylphenyl) -0,0-di-methylthiophosphate), etc.

In Western European countries, milbemycin is also used - a drug for the prevention of heartworm infection, effective in demodicosis. It is a macrolide produced by Streptomyces hygroscopicus. Its mechanism of action is to disrupt the neurotransmission of y-aminobutyric acid in invertebrates. Compared to amitraz, milbemycin shows no side effects when used at recommended dosages, including in breeds sensitive to ivermectin. The effectiveness of therapy with drugs based on it is higher than with the use of drugs whose active ingredient is amitraz (10). However, treatment with milbemycin, as well as with amitraz, is desirable to start in a hospital, so that in case of poisoning it is possible to take immediate measures, or to prescribe them together with Gamavit, which reduces the toxicity of these compounds.

In some cases, ticks develop inherited resistance to ivermectin (2). Apparently, in a number of cases observed in the USA and Western Europe, this explains the almost zero effectiveness of ivermectin in the treatment of demodicosis. However, in the treatment of generalized demodicosis, ivermectin is perhaps the only treatment for dogs that are at risk of being euthanized after their owners have exhausted the possibilities of local treatment with amitraz-based drugs.

As for "Saifli", its advantage lies in oral administration and the absence of adverse reactions, however, the course of treatment is long - up to 6 months.

Overall, generalized demodicosis in dogs remains one of the most difficult skin conditions to treat, and no new drug is guaranteed to be successful.

Demodicosis, especially the generalized form, develops, as a rule, against the background of immunosuppression. In its treatment, it is advisable to prescribe modern immunomodulatory drugs (5). Among them, Fosprenil has a certain advantage, which also has antiviral properties. It not only stimulates the immune system, correcting immunosuppression, but also has a high hepatoprotective activity - an extremely important property in the treatment of demodicosis, when the liver can function at its limit. Here, fosprenil is preferable to even Essentiale-forte: mites feed on the secretion of the sebaceous glands and multiply more actively, receiving food enriched (especially with B vitamins), and Essentiale-forte is a drug with a fairly wide range of vitamins and phospholipids. On the other hand, when using the immunomodulator Maksidin, a faster improvement in the skin condition is noted.

The use of corticosteroids for demodicosis is usually not justified, since dogs with a generalized form often develop secondary bacterial pyoderma, often threatening the life of the animal. On the contrary, to prevent the development of secondary infections, Salmosan is shown - a polysaccharide of the O-somatic antigen of Salmonella, which is used to increase nonspecific resistance.

In the scaly form of the disease, it is desirable to additionally prescribe vitamin E (flax oil, milk thistle), which stimulates skin regeneration and improves hairline.

In any form of the disease, Gamavit is indicated, which is not only an adaptogen, but also a universal detoxifier. It significantly reduces the toxicity of acaricides, and in combination with salmosan, its antitoxic effectiveness increases (4). An important indication for the use of gamavit is its antioxidant activity, which helps to neutralize the harmful effects of free radicals and toxic decay products. In addition, the introduction of gamavit normalizes the blood formula.

In any form of demodicosis, the appointment of the Gamabiol balm is indicated, which effectively relieves inflammation of the skin and subcutaneous tissue. With its appointment, even with severe extensive skin lesions, rapid healing and cleansing of the skin is observed. Apparently, the high efficiency of Gamabiol in suppressing skin inflammation is determined by the combination of polyprenols and terpenoids, which accelerate regeneration processes, have antiseptic and anti-inflammatory effects and improve microcirculation in the skin, with hyaluronic acid, which reduces the synthesis of prostaglandins, improves tissue blood supply and increases the bioavailability of other components of the drug. .

LITERATURE:

1, Vasiliev, I.K. The use of Gamabiol balm in small pets. - Zooindustry, 2008,
2, Viktorov A.V., Drinyaev V.A., Ivermectin, Development of resistance // Veterinary, No. 4, 2002, -C, 50-54,
3, Makarov V.V. Vasilevich F.I., Muravleva T.V., Soshenko L.P., Negussie B.T., Manichev A.A., Sereda SV., Molchanov I.A. Epizootology of demodicosis of dogs in modern conditions // Veterinary practice, No. 3,2000, - C, 27-35,
4, Ozherelkov SV, Vasiliev I.K., Narovlyansky A.N., Pronin A.V., Sanin A,V, The use of the drug "Salmozan" as a detoxicant in experimental conditions and when included in the treatment regimen for diseases of various etiologies of small domestic animals // XV International Moscow Veterinary Congress. 2007
5, Sanin A.V., The use of immunomodulators in viral diseases of small domestic animals // Russian Journal of Veterinary Medicine, No. 1,2005, - C, 38-42,
6, Svyatkovsky A.V. Karpenko L.Yu., Tikhanin V.V., Svyatkovskaya M.A. Zibrev 0.0, Some issues of pathogenesis and diagnosis of demodicosis in dogs // Veterinary practice, No. 1,1997, -0 40-45,
7, Semenov I.V., Buran ON, Demodicosis of dogs // Abstracts of the I International Veterinary Conference, October 1996, - Kyiv, - C, 65-70,
8, Shustrova M, V. Scabies and demodicoses of animals of different species (epizootology, etiology, pathogenesis, development of a system of measures for the prevention and elimination of these diseases in the conditions of the North-West region) // Diss, doctorate, veterinary sciences, St. Petersburg, St. Petersburg State Academy of Medical Sciences , 1996.
9, RJ. Ginel. Demodicosis in dogs. WALTHAM Focus, v.6, No. 2, 1996, p, 2-7

One of the most difficult skin diseases to treat is demodicosis in dogs. At the initial stage, the disease may not seem too dangerous: other animals and humans cannot get infected, the pet is active, the appetite is preserved, even the itching is not too strong. However, without treatment, the signs of demodicosis in dogs become more pronounced, the disease affects the internal organs and, ultimately, can lead to the death of the pet.

Read also: Seething in the dog's stomach: possible causes and methods of treatment

Ways of infection

In recent publications, one can often read that demodexes are part of the normal flora, that is, they live on the skin of any dog, far from always causing an illness. It is noted that, like some other skin diseases in dogs, demodicosis is hereditary.

Thus, there are at least two points of view on demodicosis in dogs, the causes and ways of infection. Apart from considering these mites as part of the normal flora, contact with sick animals is dangerous (that is, a healthy dog ​​can become infected from a sick one). If we start from a different point of view, the prevention of demodicosis in dogs comes down only to maintaining general health, since with a decrease in immunity and hormonal diseases, ticks begin to multiply actively.

Read also: Thyroiditis in dogs and cats: diagnosis and therapy

Forms and symptoms

Before treating demodicosis in dogs, it is necessary to determine the form of the disease:

Treatment of demodicosis in dogs: individual, comprehensive, caring

According to the features of the manifestation, pustular and scaly (squamous) forms of demodicosis are distinguished. The body is affected locally or generalized.
The scaly form is characterized by specific areas of baldness: around the eyes, lips, forehead, eyebrows, paws. In the first stage of the disease, the skin turns pink, scales, cracks, and nodules appear. In the next stage, the skin color changes to gray-blue, rounded redness appears more clearly. 25% of dogs get this form of demodicosis. You can find photos of animals with manifestations of this form on the Internet.
The pustular form is diagnosed in the presence of purple nodules against the background of swollen, reddened skin. The nodules turn into ulcers, bursting with the release of pus and blood. The disease can be complicated by the addition of an infection, then the skin wrinkles, cracks, itches, acquires a disgusting smell. 27% of animals are susceptible to this form of demodicosis.
The mixed form, which occurs in almost half of the cases, is much more difficult for animals to tolerate. Ulcers form in place of pustules. The animal constantly freezes due to a violation of thermoregulation.
The generalized form is characterized by the presence of 5 or more lesions. Such a defeat is possible only against the background of a marginal decrease in immunity in a serious primary disease, which must be identified. It is impossible to cure a generalized form of demodicosis without treating the underlying disease.
Clinical manifestations of demodicosis
The final diagnosis is made in a veterinary clinic based on the study of several scrapings from the skin. With a generalized form, some additional research, such as a biopsy, may be required.
Treatment

The disease gives the owner of the dog a lot of trouble. You can not neglect the treatment of demodicosis in dogs, hoping that the disease will pass by itself. At the beginning of treatment, the room where the animal is kept, its care items must be disinfected: scalded (the tick dies in a minute at a temperature of 50 degrees) or sprayed with 2% Sevin suspension, 0.5% Chlorophos aqueous solution or 3% Nikochloran emulsion.
Veterinarians note that none of the drugs guarantees a cure for the generalized form of glandular disease. In addition, animals have individual intolerance to certain drugs, in this they are similar to us.
With any form of demodicosis, veterinarians recommend for the treatment of Gamavit - a normalizer of the blood count, an antioxidant, an adaptogen, a detoxifier that reduces the toxicity of acaricidal agents. In combination with Salmosan, the toxic activity of gamavit increases. Balm "Gamabiol" effectively removes inflammation of the skin and subcutaneous tissue. Rapid healing of the skin was observed even with extensive lesions. Soft x-rays have also proven themselves well in the treatment of demodicosis.
For external use in the treatment, you can make home-made liniment: combine equal parts of solar oil and turpentine (or carbon tetrachloride). Rub in a day. Recovery usually occurs in half a month or a month.
Another recommended method for the treatment of demodicosis in dogs is the intravenous administration of a 1% solution of trypansini Trypanum coeruleum (dose - 0.005 g of dry matter per 1 kg of dog weight) while rubbing sedimentary sulfur powder into the affected areas. The animal will be healthy in half a month.
Generalized demodicosis is a complex general disease of the body that requires complex therapy. An individual treatment regimen is selected for each dog. Assign acaricidal, antimicrobial, antifungal, antitoxic, adaptive, immunoprotective drugs.
Of the acaricidal agents, the following drugs are recognized as effective:
based on amitraz;
ivermectin (ivomeca);
milbemycin;
tiguwon;
Dectomax
oral preparation "Syfli".
In recent years, the tick's inherited resistance to ivermectin has been noted. But with the generalized form of glandular disease, ivermectin remains the only treatment after the possibilities of drugs based on amitraz have been exhausted and the dog is threatened with euthanasia. The course of treatment of demodicosis in dogs using "Saifly" will take about six months, be patient.
Immunomodulatory drugs:
fosprenil, combining antiviral, hepatoprotective properties. The liver with demodicosis works to the limit, so its support is very appropriate;
maksidin allows you to quickly improve the appearance of the dog's skin.
cheerful dog
With any form of demodicosis, treatment should be extremely careful and consistent, your attitude should be sensitive, caring, you have no chance of making a mistake. Make sure that during treatment, the medication and skin treatment regimen prescribed by the veterinarian is strictly observed. The first thing to do is to make the dog's diet as complete as possible. Many owners are happy to report that optimal nutrition contributes to the recovery of the pet to a greater extent than medication. Vitamin E stimulates skin regeneration and improves the quality of the dog's coat, so include flax and milk thistle oil in your diet. Our pets gave us so many pleasant moments, let us thank them for this with high-quality treatment!

Tutorial

The tutorial was prepared by:

Vasilevich F.I. - candidate of veterinary sciences, associate professor;
Kirillov A.K. - Doctor of Veterinary Sciences, Professor.

The textbook is intended for students of veterinary faculties, students of the advanced training system and practical veterinarians.

The study guide gives the characteristics of the disease, systematics, morphological and biological features of Demodex canis ticks, shows the ways of infection and transmission of invasion, clinical symptoms, pathogenesis, diagnosis, immunity, treatment and prevention of demodicosis in dogs.

Reviewer - head. Laboratory of Acarology and Entomology All-Russian Research Institute of Veterinary Entomology and Arachnology, Doctor of Veterinary Sciences, Professor G.S. Sivkov.

Published by decision of the editorial board of the Russian Academy of Management and Agribusiness.

Responsible for the issue - Golik N.I., Vice-Rector for Academic Affairs, Professor.

Editor Rybalova I.G. ; Corrector Stolnikova N.Yu.

(C) Russian Academy of Management and Agribusiness, 1997

INTRODUCTION

PATHENGER

When taking material for research, along with ticks, lymph, blood, pustular fluid, purulent masses get into the preparation, that is, it is extremely difficult to obtain ticks in their pure form. With a scaly form of tick damage, it can be removed from the skin only through deep scrapings, while the preparation contains a large number of epidermal flakes, hair fragments, lymph, blood and other tissues. In addition, in an unfavorable environment, the mites of the preimaginal phases, due to their high activity, by contracting the mouse of their body, give it a shape that does not correspond to the usual ideas about it. Constrictions of the body can appear where they normally do not exist. The cuticle of the D. canis tick, especially in individuals of the preimaginal phases of development, is so thin and transparent that the possibilities of light microscopy do not allow one to observe the process of formation of the cuticle of proto- and deutonymphs in the shell of the progenitor. The shell of a new individual, which is formed in the body cavity of the predecessor, is so close to the cuticle of the latter that it is possible to differentiate the external skeleton of the new individual only during the molting of ticks.

Female. The body length of the female tick (Fig. 1) varies from 213.3 to 260.7 microns. Juveniles are smaller. Sexually mature females in the period of active oviposition are much larger (238.5±10.2 µm). The width of the body in the region of the podosome - the widest section - is 39.2 ± 3.8 μm.

Rice. 1. Female mite Demodex canis

The anterior section - gnathosoma is a complex of oral organs, equipped with a powerful head group of muscles 25.5±1.7 µm long, 27.6±2.4 µm wide. The gnathosoma consists of pedipalps, hypostome, chelicerae, and other accessory structures.

The middle, widest part of the body - the podosome has a length of 71.1 ± 6.7 microns. On its flat ventral side there is a coxosternal skeleton, four pairs of three-segmented legs and four pairs of their epimeral plates (epimer). The coxosternal skeleton is formed by the fusion of the epimeral plates of the podosome and is, in fact, the boundary formation of the epimeres. This part of the skeleton has the most dense chitin. The central trunk of the coxosternal skeleton ends with the sternal process, 4–5 μm away from its end, the vulva is located. The internal organs are located in the cavity of the podosome.

The podosoma without sharp boundaries passes into the opisthosoma, which is shaped like a cone with a rounded apex directed caudally. The length of the opisthosoma is 142.4±14.9 μm. In the opisthosoma you can see the formed egg.

The male is smaller than the female, its length ranges from 201.4 to 218.1 microns. The gnathosoma of the male is somewhat shorter, but wider than that of the female (23.8±2.2 x 29.1±1.8 μm). The podosome does not differ significantly, but its cavity contains the penis, which consists of a base, a body, and a head 31.2 ± 3.8 µm long. From the sides of the podosome of the male, at the level of the base of the penis, two or three transverse folds are visible, which provides a tick in this area. The podosome, narrowing, passes into the opisthosome, forming a constriction at the point of transition of one part of the body to another. Males have one or two deep folds at the constriction site.

The male opisthosoma is covered with a delicate transparent chitinous membrane with hardly noticeable small transverse grooves; its length is 115.6 ± 8.2 µm. The opisthosoma contains a pair of bean-shaped granular testes.

Egg. The length of the egg ranges from 68.7 to 83.0 microns, the width - from 19.0 to 33.2 microns. It has a diamond shape, covered with a delicate, transparent shell, the surface of which, when examined with a light microscope, seems smooth. The anterior pole of the egg is more obtuse, while the posterior pole is sharper and somewhat elongated.

Larva. Its length is 81.6±14.9 µm, width is 28.5±3.3 µm. The body of the larva consists of two sections: the gnathosoma and the idiosoma. The gnathosoma includes an aggregate of oral appendages consisting of underdeveloped pedipalps, chelicerae, hypostome, and some auxiliary structures. The idiosoma is nothing more than the thoracic region of the larva, which makes up the bulk of its body 67.4112.8 microns.

Protonymph. Its length is 122.2±21.4 mm. The width of the body in the area of ​​the podosome is 29.1±4.7 mm. It should be noted that the protonymph at the moment of emergence is always smaller in size than the larva during the period of stabilization of its growth. Therefore, differentiation should take into account the number of legs, the shape of the body and the presence of three sections (gnathosomes, podosomes and opisthosomes).

Deutonymph. The largest individual of the preimaginal stages of development of ticks. The average body size of a deutonymph is 201.6±50.1 x 39.1±5.9 µm. In the deutonymph, the podosome is prominent, especially its ventral surface, which bears epimeres, the fourth pair of legs and the transverse striation of the cuticle of the entire body are clearly visible. The opisthosoma looks like a short tail. On the ventral side of the podosome, a coxosternal skeleton is clearly visible, which is absent in the protonymph.

Thus, sexual dimorphism in the tick D. canis is pronounced at the adult stage. The female is larger than the male, and the male has a much shorter opisthosome. When differentiating a male from a female, body shape should also be taken into account. If in the female the gnathosoma, expanding towards the base, smoothly passes into the podosome, and the latter, gradually narrowing backwards, smoothly passes into the opisthosoma, which makes the body of the female as a whole look truly worm-like, then the male clearly has a more voluminous middle part - the podosome. At the point of transition of the podosome into the opisthosome, the male has a clearly expressed constriction of the body. However, the main distinguishing feature is the presence of a penis in the male, and the vulva in the female. In the opisthosoma, a pair of testes is found in the male, and an egg that is forming or ready for laying is found in the female.

A truncated demodectic mite has also been described in the dog, associated with generalized desquamative pruritic dermatitis (20). This species is probably a permanent resident of the skin, similar to the unnamed species described in the cat (21). Whether this shortened form represents a new species is unknown.

Life cycle of the D. canis tick

Information about the biological characteristics of these mites is scarce and contradictory. An analysis of the literature data on the development cycle of D. canis ticks indicates that ticks go through the following phases during ontogeny: eggs, larvae, protonymphs, deutonymphs, and adults (Scheme 1, 2). Embryonic development inside the egg lasts from 2 to 4 days. Postembryonic development is characterized by the fact that individuals of the preimaginal stages of development go through two states: active and passive. Being in the active state, the larva, protonymph and deutonymph are outwardly active. They feed heavily, grow and develop. Upon reaching the largest size for the active state, the engorged larva, tarot-to-deutonymph, pass into the passive state. They begin the restructuring of the body, which is composed of two interdependent processes - histolysis and histogenesis. The essence of histolysis lies in the disintegration of the internal organs of the tick, and histogenesis - in the creation of tissues and organs of an individual of a new stage of development in the body cavity of the predecessor. Histolysis also captures the muscular system. Therefore, during the restructuring of the organism, the larva and both nymphs become completely immobile and do not need food.

Scheme 1. The life cycle of the Demodex canis tick (according to V. A. Sokolovsky) O - egg; L - larva; N - nymph, J - imago, p - mobile, np - motionless

EPIZOOTOLOGICAL FEATURES

Demodicosis has been known since 1843 as a special form of canine scabies.

Lifka, Gmeiner, Gruby, it was called red scabies, small rash, hereditary scabies (18, 25).

In Russia, there are only a few works dealing mainly with the morphology and biology of D. canis ticks (4. 6, 8, 9). The data of the veterinary reporting of the city veterinary services testify to the wide spread of demodicosis in dogs.

SV Larionov (6) during the examination of 658 dogs with skin lesions in 226 (345%) found demodicosis.

MV Shustrova (11) in St. Petersburg examined 1115 dogs, of which 725 were diagnosed with demodecoe.

Despite the widespread occurrence of demodicosis, the issues of epizootology and pathogenesis have not been studied so far, and effective measures to combat this invasion have not been developed.

When studying the literature, we were faced with the question of what studies are based on the assertion of many authors that D. canis is a normal inhabitant of the skin of dogs.

In 1910, Gmeiner, based on the histomorphology of the skin. installed. that D. canis mites are not found in healthy dogs (18).

F. Lifka (25) objects to him. He tested 50 dogs with "clear skin" and only one 2-month-old bassist was able to detect mites on a sample from the upper and lower lip. He suggested that he was dealing with the onset of the disease. The author concludes that mites are not permanent inhabitants of the skin of healthy dogs.

M. Gaafar (16) conducted a study of 93 dogs of different breeds aged from 2 weeks to 11 years without clinical signs of skin lesions. The material was taken from the skin of the upper eyelid and from the temple area. In 5 cases, the D. canis tick was found.

F. Koutz (24) examined the skin of 204 healthy dogs aged 3 months and older. up to 12 years old. Samples were taken from the upper eyelid, upper and lower lips, cheeks, etc. The D. canis tick was found in 108 dogs.

F. Piotrowski et al (36) in their experiments took samples from the same places as P. Koutz. Of 100 test dogs, 39% were found to have D. canis ticks. Their age ranged from 4 weeks to 8 years.

Us in the period from 1983 to 1993. in Moscow and the Moscow region as a result of microscopic examination of skin scrapings from the lips. eyelids, forehead, cheeks, inner thighs, axilla and udder from 415 dogs with no visible clinical signs of skin lesions, only 36 or 8.6% were found to have D. canis mites. In 18 dogs, ticks were found on the eyelids, in 9 - on the cheeks, in 8 - on the lips, in 6 - on the vertebrae, in 2 - on the inner surface of the thighs. The dogs were usually purebred. 16 dogs were younger than 1 year old, 9 were from 1 to 3 years old and 11 were older than 3 years old.

In addition, in 1994 we examined the skin of 25 dogs after their death. During life, they had no signs of skin lesions. The skin removed from the dog was abundantly moistened with water, then rolled up and placed in a plastic bag for 4-5 days. During this time, the hair fell out due to rotting of the skin and the epidermis was easily scraped off. Samples were taken from 25 sites, placed in 10% KOH and examined under a microscope. As a result, D. canis mites were found in 2 dogs (8%), and all dogs were older than 5 years of age.

We believe that this method is more accurate as a larger area of ​​skin can be tested.

Thus, statements or assumptions often found in the literature that D. canis mites can be considered as normal inhabitants of the skin of dogs are not confirmed by our studies, because it is almost impossible to answer the question of whether there is a carrier or the onset of the disease. To further clarify this issue, it is necessary to conduct a study of the entire skin using histological experiments.

Gowing (20) notes that of the 507 dogs affected by demodicosis, all age groups under the age of 12 years were represented. Almost 2/3 of his patients fell ill in the first year of life, the proportion of dogs older than 5 years was 35 cases.

C.Olschewski (32) believes that older dogs are more likely to get tumors, they are treated with corticosteronds, which weaken the immune system and they are more susceptible to demodicosis.

SV Larionov (6) notes that out of 226 dogs affected by the D. canis tick, only 44 (19.5%) were older than 2 years.

D.W.Scott (39) did not establish a clearly expressed age-related dynamics in this invasion.

In our studies, out of 61 dogs infected with demodicosis, the maximum incidence rate was observed in animals aged 6 months and older. up to 1 year - 42.3%. or 260 dogs, in 191 cases (31%) demodicosis was registered at the age of 2 to 6 months. At the age of 1-3 years - 93 cases (15.1%), older than 3 years - 61 cases (9.9%).

The high incidence of dogs under the age of 1 year is probably due to the fact that at this time the animals are exposed to all kinds of stressful situations (vaccinations, ear cropping, teeth changing, etc.), which certainly weakens the body's defenses.

In 2.4% of cases, we observed demodicosis in 1-2-month-old puppies. At this age, there are practically no contacts with other dogs, and it is not difficult to assume that the infection came from patients with demodicosis. mothers.

Gender distribution

Koutz (24) identified 280 females and 247 males among 507 patients with demodicosis.

Olschewski (32) notes that of 147 dogs admitted to the Giessen clinic with a diagnosis of demodicosis, 103 were males and 44 were females.

SV Larionov (5, 6) - out of 226 dogs with demodicosis, 114 (50.4%) were females.

In our study, out of 615 dogs diagnosed with demodicosis, 281 (45.6%) were females (1, 2, 3).

Numerous reports in the literature and our own studies allow us to conclude that pedigreed dogs are much more likely to get demodicosis than outbred dogs.

Koutz (24) found that out of 507 cases, demodicoe was present in 42% of longhaired and 58% of shorthaired dog breeds.

W.H. Miller (28) notes that Dobermans, dachshunds, English bulldogs, Boston and Staffordshire terriers, hounds, rottweilers, pinschers, etc. are more likely to suffer from demodicosis.

F. Reichert notes that out of 18325 dogs, in 1921-1923. treated in the Dresden clinic, 1342 dogs suffered from demodicosis. The author categorizes them by breed as follows: Fox Terriers, Miniature Pinschers, Rottweilers, Boxers, Dobermans, German Shepherds, Schnauzers, Airedales, Great Danes, etc. (quoted from Olschewski (32).

S.V. Larionov (6) notes a slightly greater predisposition to demodicosis in short-haired dog breeds (61.9%), and the author explains this by the better development of their sebaceous glands.

The results of our studies showed that the majority of dogs with demodicosis were purebred (90.6%) and only in 37 cases (6.01%) were mixed and outbred (Table 1).

Table 1 Distribution of dogs with demodicosis by breeds

Identified patients

East European Shepherd

German Shepherd

bull terrier

doberman

Rottweiler

staffordshire terrier

English bulldog

French Bulldog

English Cocker Spaniel

American Cocker Spaniel

Mongrel and crossbreeds

Other breeds

The seasonal dynamics of demodicosis looked as follows: in winter - 291 (47.3%), in spring - 240 (39.02%), in summer - 46 (8.5%), in autumn - 30 (4.9%). The wide distribution of demodicosis in the winter-spring period is obviously associated with a decrease in skin tone in animals due to insufficient insolation, which causes the activation of ticks and, as a result, the clinical manifestation of the disease.

Trautwem (40) placed material from a dog with severe demodicosis in a saline saline solution, then applied it to healthy puppies. There was no clinical manifestation of the disease (observation for 6 weeks), however, D. canis mites were found in skin scrapings.

E. Enigk et al (23) conducted experiments on the passage of ticks through the skin in puppies at the age of 3 months. The experiments were successful. Material containing ticks was applied to shaved areas in the back and fixed with adhesive tape (6-12 weeks). After 6 months one dog was found to have a squamous form. In two other animals, mites were found on the skin of the back.

S.M Gaafar (16) used 6 purebred Beagl puppies obtained from SPE mothers or by caesarean section. The infected material was applied to the forehead area. After 3 days, pustular form and mites were found in 3 animals.

D.W. Scott (39) describes a kenneled dog that had no clinical signs of demodicosis other than a sparse coat, but all puppies from her two litters developed demodicosis at 3-5 months of age.

Unfortunately, we did not find works devoted to this problem in the domestic literature.

During 1988-1992. we examined 12 litters of dogs of various breeds (long-haired to short-haired). Seven litters were taken from clinically healthy mothers, and 5 dogs suffered from demodicosis. Ticks were found in 8 litters, 4 litters from demodicosis females and 4 from dogs in which demodicosis was not clinically manifested (Table 2)

Table 2 Results of examination of dogs for demodicosis

dog number

demodicosis

Number of puppies in a litter

Examined

results

Found D. canis

Not found

Analyzing the data in Table 2, we see that infection with demodicosis occurs in the first 3 months of life. In the future, an increase in hair length and keratinization of the epidermis of the skin greatly complicates the resettlement of ticks. Long hair is probably an insurmountable barrier to the movement of the slow moving D. canis tick. Since, regardless of the breed, the puppies have short hair after birth and the udder of the bitch is covered with sparse hairs, there is always direct contact with the skin and the mechanical obstacle to the passage of the tick is minimal. Under the influence of a significant thermal irritation, which is carried out through close contact between the puppy and the female, the habitat of the ticks changes. They leave the female's hair follicles and pass on to the pup.

PATHOGENESIS

The pathogenesis of demodicosis in dogs is not entirely clear, especially in the chronic and generalized form.

With demodicosis, the individual predisposition of the animal to this disease is expressed. It is associated primarily with a violation of the physiology of the hair follicle, which is observed during hair loss (during molting, for example), or lagging behind the walls of the hair follicle from the hair root (skin atony). This allows the mite to easily penetrate the hair follicle. However, in dogs, mites can sometimes enter an intact follicle.

Another predisposing factor may be associated with suppression of immunological reactions in the skin, as well as high levels of corticosteroid hormones or very low levels of thyroid hormone. These hormonal disorders negatively affect skin immunological reactions.

Infection of susceptible animals can occur only by contact and only by sexually mature forms of the tick, which are selected from the follicles to the surface of the skin and actively move along it. At this time, they breathe through the trachea (a type of ancestral breathing) (6).

Most often, demodicosis lesions are localized in places where the skin is more elastic, there are more folds and, consequently, there is more moisture in the skin layer of the air. Areas of the body that are most active upon contact (head, chest) are more often affected.

The initial stage of the pathogenesis of demodicosis is the penetration of the flare into the hair follicle.

Two parts are distinguished in the hair - the root, which is hidden in the hair follicle, and the shaft. The hair follicle is a cavity, the walls of which consist of inner and outer epithelial (root) sheaths and a connective tissue bag. Below the hair root has a thickening called the hair bulb. This place, in fact, is the place of hair growth. From below, a hair papilla, rich in blood vessels, protrudes into the hair follicle, nourishing the hair. Slightly above the bulb are the sebaceous glands, which in dogs belong to the tubular alveolar glands. The excretory ducts of these glands open at the top of the hair follicle. The sebaceous glands produce sebum. which gives the skin softness and elasticity.

There are several options for the penetration of the tick into the follicle. The easiest option is when there is no hair in the follicle. This happens when shedding, hair growth disorders, etc. In this case, the tick freely crawls into the follicle and descends deep into it. It is somewhat more difficult for a tick to penetrate into the follicle where there is hair, but due to skin atony (decrease in skin tone), the outer root sheath is detached from the hair. The tick penetrates the lumen of this detachment and moves deep into the follicle

Not the last role is played by the presence of pyogenic microflora and, above all, staphylococci, which are found in large numbers in the affected areas (4). Using electron microscopy, it was shown that the tick from the lesions is literally completely covered with these microorganisms.

As a rule, the destroyed cells of the host organism are replaced by new epitheliocytes, and usually the furrows are overgrown. However, if the entire epithelial lining of the demodicosis focus is destroyed, up to the basement membrane, then the host organism responds to this in the following way. The location of the basement membrane is shifted deep into the underlying connective tissue, and the epithelial lining is restored. Such a displacement of the basement membrane allows ticks to win back their living space, thus increasing the size of the demodectic focus and the receptacle for individuals of the entire colony. This process can be repeated many times. The larger the receptacle (the conquered living space), the more nutrient substrate is formed due to the epithelial tissues of the host.

Bags of the hair follicle hypertrophy, turning into a connective tissue sheath of the demodicosis focus, and the outer root sheath transforms into its epithelial lining. Destruction of the epithelial layer and hypertrophy of the size of the sebaceous gland lead to the loss of the ability to produce its own secret - sebum.

Thus, the D. canis mite, penetrating into the follicle, destroys the epithelial layer, which serves as a nutrient substrate for it (and also for its offspring). As a result of its activity, a demodectic focus is formed at the site of the follicle, containing a colony of ticks.

Numerous literature and experimental data indicate that long-term and severe dermatitis is accompanied by impaired liver function (2-4), which can be detected using biochemical diagnostics. Conducting biochemical studies in the treatment of animals with demodicosis is important, in particular, when prescribing drugs that have a hepatotoxic effect. In addition, biochemistry data will make it possible to find out whether liver pathology is a predisposing factor in demodicosis.

According to M.G. Podagretskaya et al. (1989), in 62% of people with demodicosis, changes in the functional state of the gastrointestinal tract and liver were detected.

In our studies, the level of leukocytes in localized lesions did not change significantly, however, when ranking, only 4 out of 15 dogs were within the normal range. Others had leukocytosis (up to ^^xK^/l). In 92% of animals with generalized demodicosis, a significantly high average value of this indicator for the group was recorded. In the leukocyte formula, eosinophilia, lymphopenia, monocytosis were noted. In animals with generalized demodicosis, a decrease in hemoglobin content, erythropenia, and an increase in ESR were noted.

Biochemical studies revealed changes in serum biochemical liver tests in 66.8% of dogs with demodicosis invasion, characterizing disorders in the hepatobiliary system.

48.3% showed signs of cytolysis, expressed by an increase in liver-specific enzymes (aminotransferases, aldolase, lactate dehydrogenase) and hyperbilirubinemia. In 25% of dogs, signs of cholestasis were recorded (increased activity of gammaglutamyl transpeptidase, cholesterol, bilirubin, bile acids).

In 21.3%, signs of mesenchymal-inflammatory syndrome (hyperproteinemia, dysproteinemia with a decrease in albumin and a pronounced increase in gamma globulins, sometimes in combination with a P-fraction) were detected. A decrease in the amount of albumins, cholinesterase, cholesterol and urea, used as indicators of hepatocellular insufficiency, was noted only with generalized pyodemodecosis (Table 3).

Table 3 Relative content of protein fractions of blood serum (%) in dogs (P<0,05)

Protein fractions

Control
(n=10)

Form of the disease

Localized
scaly
(n=8)

Generalized
scaly
(n=5)

Pyodemodecosis
(n=5)

Albumins

Globulins:

Alpha1

The content of total protein increased depending on the severity and duration of the disease. So, in dogs with a generalized scaly form, it was significantly higher than in controls, by 1.23 times, and in animals with pyodemodecosis - by 24%. The decrease in the relative content of albumin was characteristic of the chronic generalized form of demodicosis, and in dogs with pyodemodecosis it was more intense than in the squamous form.

A significant increase in a1-globulins in all sick dogs indicated that they had inflammation.

The increase in this fraction is associated with increased synthesis of immunoglobulins and their accumulation in the blood serum.

In dogs with demodicosis, a significant increase in the concentration of immunoglobulins of the G(lgG) class was found with an almost unchanged level of IgM. Therefore, hypergammaglobulinemia, characteristic of demodicosis, was caused not by autoimmune processes in the liver, but by the activation of the humoral immune response to the antigens of the Demodex canis tick and its waste products (1).

Comparison of the data of functional liver tests allows us to conclude that with generalized pyodemodecosis there is a serious violation of liver function, requiring pathogenetic therapy.

SYMPTOMS

There are many reports in the specialized literature that characterize the clinical picture of canine demodicosis. Moreover, most authors distinguish two forms of skin lesions in demodicosis: squamous and pustular.

SV Larionov (5.6) described papular as a rare form of demodicosis in dogs.

Analyzing the literature data and our own experience, we distinguish the following forms of demodicosis in dogs:

1. The scaly (squamous) form (Fig. 2) is observed in 145 heads (23.7%). It is characterized by the presence of rounded, hairless areas of skin ranging in size from 1 to 20 mm in diameter, located on the superciliary arches, forehead, nose, lips, limbs. With constant hair loss, rounded, bald spots are formed, which can be sharply limited. At the same time, there is a slight reddening of the skin, the formation of bran-like scales on it, the skin can be rough, crack, and sometimes small nodules form. Along the edges of the focus, the hair is weakly strengthened, brittle, unevenly located. In a later stage, the skin may be bluish-gray with rounded redness.

Lesions in squamous form of demodicosis

A) ventral surface

B) dorsal surface

2. Pustular form (pyodemodecosis) (Fig. 3). It was observed in 161 dogs (26.2%) and it developed as if from squamous. and independently, and in 45 dogs (20.1%) it was generalized. In the pustular form of demodicosis, the skin was usually swollen, reddened, with small hard nodules that appeared next to the hair follicles and had a blue-red tint. The nodules quickly turned into yellow, red-brown, and sometimes blackish pustules. Under light pressure, sebaceous pus was released from the abscess, sometimes with blood, in which there were ticks at all stages of the life cycle. Due to secondary infection, extensive pyoderma occurs with the formation of ulcerative abscesses. The skin becomes thick, wrinkled, moist, and often cracks. Itching is often very strong, the smell is unpleasant.

Table 4 Distribution and localization of skin lesions in dogs with demodicosis

Areas of lesions

Number of animals n=615

Muzzle, lips, eyes, front paws

Nostrils, eyes front paws, withers shoulder blade

Nostrils, eyes, neck

Nostrils, eyes

Erythema presence

Absence

Itching presence

Absence

Pyoderma presence

Absence

With pyodemodecosis, in almost all cases, we observed an increase and soreness of the submandibular lymph nodes, often purulent phlebitis of the extremities, lameness

In 9 cases (1.46%) there was a papular form. Papules were located in the dorsal region of the sacrum of the tail root. Their sizes were from 2 to 7 mm in diameter, very dense. Puncture of the papule wall contained, as a rule, dead mites or their fragments (limbs, coxosternal skeleton, gnatosomal structures, etc.). On the surface of large papules, the hair was somewhat thinned but preserved.

Most often (300 cases or 48.7%) there was a mixed form of demodicosis (Fig. 4). Moreover, with this form, the disease proceeded most severely. In bald areas, the skin is heavily wrinkled, which gives it a corrugated appearance. In place of the opened pustules, ulcers often form. Due to a violation of thermoregulation, the dog experiences chills even in a warm room. Such cases usually end in death.

We believe that demodicosis of the paws should be singled out as a separate form as a common disease in English and American Cocker Spaniels, manifested by erythema, cellulitis, furunculosis and hair loss, and in severe cases, we observed purulent phlebitis of the veins of the limbs and severe lameness, as well as otodemodecosis when the inner surface of the auricles is hyperemic, small nodules appear on it, while the auricles are swollen, hot to the touch, painful, there are many mites in scrapings at different stages of development. Abundant formation of ear wax and the appearance of crusts are also characteristic.

In some cases, a generalized form of demodicosis occurs (Fig. 5)

PATHOMORPHOLOGICAL CHANGES IN THE SKIN OF DOGS WITH DEMODECOSIS

macroscopic changes. Pathological changes in canine demodicosis have not been studied enough and are very controversial. Demodicosis in dogs occurs in two forms - squamous and pustular. The first form is characterized by the formation of alopecia and wounds. The demodicosis process begins with the head and paws, gradually spreading to the entire surface of the animal's body. Changed areas of the skin, as a rule, are dry, with a flaky coating of gray-white color. In places of defeat, baldness, thickening of the skin and the formation of folds are noted. Often there are scabs of dark red color of soft consistency in the form of crumb-like masses. Their number and size depends on the intensity of the invasion.

Skin samples from different sites of the lesion, pieces of lymph nodes, liver, kidneys, and spleen, were fixed in a 40% neutral formalin solution, embedded in paraffin, and serial sections of 6–8 μm thick were prepared, stained with gsmatoxylin and eosin, as well as by Wang Gieyun.

When examining the skin of dogs affected by the D. canis mite with a pustular form of the lesion, some distinctive features were found.

Tissue changes in the skin of dogs with demodicosis were very diverse. They were detected in the epidermis, hair follicles, nipple and secular layers of the dermis. The muscles remain intact. The stratified squamous epithelium is ulcerated and flattened in limited areas. Purulent-necrotic or necrotic masses are determined on the surface of these areas. Many orifices of epithelial hair follicles and hair follicles are enlarged, contain flakes and destroyed epithelial cells, in the stratified squamous epithelium and the orifices of hair follicles there are foci of hyperkeratosis and parakeratosis. Around the follicles with the accumulation of mites and the preserved wall of the outer root sheath, the cellular inflammatory reaction is very weakly expressed or absent (Fig. 6).

With the destruction of the wall of the hair follicle and. contact of mites with the dermis, a cellular inflammatory reaction develops in it, informing epithelioid granulomas with the presence of giant multinucleated cells of the Pirogov-Langans type and foreign bodies. In the turf, both massive inflammatory infiltrates and foci of various sizes of granulomatous structure are determined. In areas of skin with necrosis in the epidermis, an inflammatory infiltrate is predominantly detected, consisting mainly of granulocytes with a predominance of eosniophilic leukocytes, among which egopgelchemia and giant cells, as well as mites, are found. The infiltrate is located in the papillary and reticular layers of the dermis. In most cases, granulomas are formed in the dermis around the mites, which consist of epithelioid and giant cells with an admixture of lymphocytes, histiocytes, monocytes, plasma cells, and eosinophilic leukocytes.

Analyzing histomorphological changes in the skin, we see. that individual mites penetrate the epidermis, where purulent-necrotic inflammation develops in their place with a predominance of granulocytes. Single mites can penetrate directly into the papillary dermis, where a granuloma develops around them, consisting mainly of epithelioid cells with the presence of giant multinucleated cells. We did not find ticks in the sebaceous glands. The sebaceous glands, as a rule, were involved in the inflammatory process for the second time and were destroyed partially or completely.

In the squamous form, we noted necrosis of the follicular wall. In this case, the hair follicles take on various forms: spindle-shaped, bottle-shaped, glass-shaped, they often atrophy.

The epithelial cells of the inner and outer root sheaths are reduced.

The epithelial cells of the basement membrane of the epidermis are deformed, lie randomly, without forming a structure characteristic of this layer. The cytoplasm is stained basophilically, swollen. The nuclei are barely visible - karyolysis. In some cases, the nucleus is absent, and chromatin clumps of various sizes are found in the cytoplasm, freely lying in the cell - karyorhexis. Cells of the prickly, granular and horny layers - in the form of homogeneous, dull, oxyphilic strips. Sharply expressed rejection of the epidermis with exposure of the surface of the papillary layer of the dermis.

The most characteristic changes in the papillary and reticular layers appear as an accumulation of cellular elements. The connective tissue basis of these zones is infiltrated mainly by lymphoid, plasma cells and fibroblasts. Among these cells, there are eosinophils, macrophages, multinuclear symplasts, and sometimes stab neutrophils. The number of cells in different histosections varied from insignificant to extensive accumulations. The latter were especially often found under the epidermis and near the affected hair complexes. Insignificant accumulations of lymphoid cells with an admixture of erythrocytes were noted near hyperemic vessels, sweat glands, and also in places of hemorrhages.

Vascular changes in the dermis are represented by persistent expansion and plethora of the entire microcirculatory bloodstream - arteriodes, precapillaries, capillaries and venules. Proliferation of intima and adventitia cells was observed, and sometimes in combination with destructive changes in the vessel wall. Spaces not stained with hematoxylin and eosin were noted near the derivatives of the skin and blood vessels.

Morphological changes in the subcutaneous tissue are manifested in the form of circulatory disorders - desolation of large arteries. Veins, capillaries and precapillaries are dilated and overflowing with erythrocytes, which merge into one continuous mass, on the border with the mesh layer and near the vessels - the presence of hemorrhages.

Summing up the histological changes in the skin with a mixed form of damage to the hair follicles and sebaceous glands, it should be said that they are characterized by necrosis of the epidermis and its desquamation. Changes in the dermis are expressed by dystrophy of collagen fibers, necrosis of hair follicles and sebaceous glands. Necrosis, as a rule, occurs as a result of prolonged mechanical and toxic effects of mites on cells.

On the basis of the conducted studies, we believe that the pathomorphogenesis in the squamous form of demodicosis proceeds in four stages.

The first stage is the introduction of mites into the hair follicles. It is characterized by hypertrophy of the inner and outer root sheaths of the hair follicles, as well as the epithelium of the excretory ducts and acini of the sebaceous glands. Hyperkeratosis and parakeratosis are noted in the epidermis.

The third stage is the defeat of the hair complexes. The follicular wall of the hair follicles and the basement membrane of the sebaceous glands in the hair complex swell and dissolve, forming cavities. D.canis migrates from such lesions to other hair complexes for further reproduction or to the connective tissue of the dermis, where the mites die and granulomas form around them (Fig. 7). The epidermis desquams in layers to the papillary dermis.

The fourth stage is the outcome. With a favorable course, the regeneration of the epidermis in the first two stages occurs rapidly due to the remaining epidermocytes between the dermal papillae. In the case of complete destruction of the epidermis, the dermis is covered with a new epidermis by centripetal growth starting from the edges of the lesion. At the third stage, when deep violations of the morphofunctional state of the skin are expressed, regeneration begins with the formation of a scab, consisting of blood, tissue fluid and damaged skin tissues. Under the scab, granulation tissue is formed. The process of epithlisacin of the affected surface is associated with an outbreak of mitotic activity of epidermal cells around the lesions. The newly formed epidermal regenerate coincides with the formation of the argyrophilic basement membrane, and with the onset of its occurrence, the granulation tissue is replaced by a coarse fibrous dense connective tissue of the codlagen type - a scar. The scar is rebuilt according to the structure of the dermis. At the same time, hair and glands begin to form in the regenerate, and it gradually acquires (over several months) the structure of normal skin. With an unfavorable course, the structure of the skin is not completely restored.

HISTOMORPHOLOGY OF THE INTERNAL ORGANS OF DOGS IN DEMODEKOZK

Lymph nodes. In the cortical substance of the lymph nodes with generalized pyodemodecosis, demodectic mites are found. They are located in the marginal and cortical sinuses and peripheral areas of the lymphatic follicles. At the site of their introduction, granulomatous inflammation develops with the presence of giant multinucleated cells. The cellular infiltrate contains monocytes, histiocytes, lymphocytes, macrophages with an admixture of eosinophilic and neutrophilic leukocytes. In a small amount, epithelioid cells and multinucleated giant cells of the foreign body type and the Langhans type are found, which are located in the peripheral areas of the granuloma. In the lymphatic follicles in the cortical layer, there are multiple, large, with wide light centers of reproduction and fission figures, cells. Pulp cords contain a large number of plasma cells. There are many macrophages in the cerebral sinuses, there are also histiocytes, lymphocytes, granulocytes,

Thus, the causative agent of demodicosis with tuberculoid-type granulomas formed around ticks with the presence of epithelioid and giant multinucleated cells is detected in the tissue of the lymph nodes. In the lymph nodes there are signs of a cellular immune response with histiocytosis of the sinuses and hyperplasia of the lymphoid follicles.

Liver. Histological examination of the liver in all cases, we noted the same type of changes. They are focal in nature and localized mainly in the portal tracts, periportally and perivascularly. The portal tracts are markedly dilated with edema, hemorrhage, and mild cellular infiltration consisting of lymphocytes, histiocytes with an admixture of eoeinophilic and neutrophilic leukocytes, and multinucleated giant cells. In the peripheral parts of the lobules, there is a violation of the beam structure of the liver, edema, hemorrhages, necrosis of groups of hepatocytes. The parenchyma contains granulomas consisting of lymphoid-histiocytic elements, epithetioid cells, and a small number of eosinophilic and neutrophilic trajajucytes. Perivascularly there are infiltrates in the form of small accumulations of lymphocytes, histiocytes and plasma cells. The hepatic cells are in a state of proteinaceous (hydrophobic and balloon) dystrophy, which has a diffuse character. Demodecoena mites were not found in the liver structures, although they can penetrate from the skin into the lumen of large blood vessels and enter the liver. A form of acute inflammatory response to ticks is the development of hemocirculatory disorders in the liver and granulomatous hepatitis with the formation of tuberculoid-type granulomas. In the development of granulomas, sensitization processes and associated immune responses most likely play a role.

Kidneys. In the kidneys, hemocirculatory disorders are found, expressed in uneven plethora of the cortical in the brain zone, a noticeable expansion of the vessels of the juxtamodular zone, edema and hemorrhages around some of them and focal fibrosis of their wall. Renal glomeruli have different diameters. Glomeruli of small diameter contain a small number of empty capillary loops. There are glomeruli with single capillary loops or with their complete absence. The extracapillary space of a part of the glomeruli with a large diameter contains a pink proteinaceous fluid. The epithelium of the convoluted tubules is in a state of granular and small-focal hydropic dystrophy. In the tubules of the medulla, small, few calcified cylinders are determined. The causative agents of dsmodecosis in the renal parenchyma are not detected.

The detected changes in the kidneys suggest that demodectic mites can cause hemopirculatory disorders, stenosis or obliteration of blood vessels, glomerular collapse and nephropathy.

Thus, in the morphological study of the skin of dogs with demodicosis, it was found that mites cause focal dystrophic, necrobiotic and necrotic processes in it. The nature of these changes depends on the intensity of the invasion and the form of the disease, and the inflammatory process is productive. In addition, in most cases, there is damage to the microvasculature and connective tissue. The sebaceous glands, as a rule, are involved in the inflammatory process for the second time; demodectic mites were not found in them.

Histomorphological examination of the lymph nodes, liver, kidneys and spleen found that mites can penetrate into the lumen of large blood vessels and enter these organs. In this case, there is a local circulatory disorder and granulomatous inflammation with the formation of non-caseating granulomas of the tuberculoid type. Once in the kidneys, mites calcify and are excreted from them in fragments.

Not destroyed mites, as well as mites outside the granulomas, are not found in the internal organs.

DIAGNOSTICS

Demodicosis is usually easy to diagnose by taking a few deep (blood-stained) scrapings of the skin, while the skin should be squeezed from the sides with your fingers to expel the mites from the hair follicle. An acarogram (count of eggs, larvae, nymphs and adults) is necessary to confirm the diagnosis, because the occasional mite can be found in skin scrapings from clinically healthy dogs (15,19).

If the found tick is random (usually 1-2 individuals in the scraping), then the skin scraping should be repeated in other places, and especially in the muzzle and paws.

With a localized form of demodicosis, it makes sense to take a scraping from healthy skin; a large number of mites may indicate the danger of subsequent generalization (15, 17.20).

In advanced cases with lichen-like and fibrotic lesions, especially in the paw region, the diagnosis can be made by microscopic examination of the biopsy material (19).

IMMUNITY

One of the most important areas in the study of skin diseases is the issue of immunity. Knowledge of the intimate mechanisms of the immunological restructuring of the body is not only theoretical, but also of great practical importance for a reasonable approach to the development of means of specific diagnostics, prevention and therapy.

The skin of dogs is a unique organ. With a thickness of only a few millimeters, it nevertheless represents the largest organ of the body. The various highly specialized cells that make it up are combined into complex structures and subsystems (Fig. 8).

One of the most remarkable functions of this organ has recently been discovered: the skin has proven to be an integral and active component of the immune system. The genetic and structural similarity of the epidermis and thymus was established.

The nature of immunologically active skin cells became clear after it was established that Langerhans cells, small populations of dendritic cells in the epidermis, are responsible for developing an immune response to locally applied antigen. Experiments conducted on mice have shown that keratinocytes are also an important element of the immune system. They not only ensure the formation of a protective keratin layer and hairline on the surface of the body, but also produce hormone-like substances that can actively influence the functioning of T-lymphocytes that enter the skin. Their potential influence on T-lymphocytes is extensive: from the regulation of maturation to the enhancement of a specific response to antigens.

Cellular and molecular reactions of the skin as an immune subsystem can be summarized as shown in Fig. 9. The antigen binds to two types of dendritic antigen-presenting cells of the epidermis - Langergavs and Greystein. Langerhans cells "represent" the antigen with a specific T-helper, which gravitates towards the epidermis during migration. Grainstein cells interact similarly with T-suppressors. Helper and suppressor responses are approximately in balance, but normally the helper (positive) signal predominates, providing an adequate response to a potential harmful foreign agent penetrating the skin. If Langerhans cells are damaged, for example, by ultraviolet light, or are bypassed (assuming that some antigens directly interact with the suppressor cycle), there will be a predominance of the inhibitory signal.

In addition to the antigen presented to it, the T-cell, programmed to respond to it, receives a second, additional signal in the form of IL-1 (interleukin-1), coming from keratinocytes. This induces the T-lymphocyte to secrete IL-2 (interleukin-2), which binds to other T-cells of the same specificity and causes them to proliferate.

As a result, the number of T-cells that are ready to resist the antigenic attack increases sharply; they pass into the lymph and carry it through the body.

The immune response in dogs with demodicosis is not fully understood. especially in the chronic generalized form of the disease. However, the apparent predisposition of some breeds to generalized demodicosis, the opportunistic nature of D. canis and the association between the disease and debilitating factors such as helminthiasis, estrus, puppies, endocrine disease glucocorticotherapy and chemotherapy, suggest a combination of hereditary predisposition and immunosuppression (6. 12, 13, 14).

Some earlier reports have supported the role of an abnormal cellular immune response as the initial cause of the disease.

First, these lesions may have been experimentally induced in puppies by administration of anti-lymphocyte serum (12).

Second, dogs with generalized demodicosis showed severe suppression of the T-cell response (15), as well as attenuation of the delayed-type skin response to various T-cell mitogens.

However, Barta et al. (13) found that the observed T cell suppression was more closely correlated with the size of secondary pyoderma and was absent in dogs with untreated demodicosis.

It has recently been confirmed that immunosuppression associated with generalized demodicosis. not associated with pyoderma.

Baring Proved Immune Suppression Is Not a Requirement for Dogs to Develop Clinical Demodicosis

Immune suppression is therefore a consequence rather than a cause of generalized demodicosis. This may explain the low incidence of demodicosis in dogs due to some of the immunosuppressive factors causally associated with demodicosis, such as neoplasms, liver disease, diabetes mellitus, and others (26).

Current information confirms that an inherited defect in D. canis-specific T cells could play a central role in the pathogenesis of generalized demodicosis. This defect can occur alone or in combination with certain immunosuppressive factors and promotes proliferation of ticks and the onset of generalized T cell depression, predisposing to secondary pyoderma and subsequently suppressing both cellular and humoral immune responses.

Unfortunately, the quantitative characteristics of immunoglobulins and their role in the pathogenesis of canine demodecoea have not been presented so far.

We determined the quantitative content of immunoglobulins in the blood serum of dogs in the norm and with demodicosis (Table 5).

Immunoglobulins of classes IgG and IgM were isolated from blood serum by anion exchange chromatography and gel filtration using sorbents gives Oyopearl -650/S/ Japan. The purity of the obtained results was controlled by the methods of immunoelectrophoresis with antisera to the proteins of the blood serum of dogs and electrophoresis in SDS-PAGE. Immunochemically pure immunoglobulins were concentrated with polyethylene glycol, the concentration of total protein in them was determined and used in further work.

Table 5 Immunoglobulins in the blood of dogs with demodicosis

Indicators mg / ml

animal groups

total protein

Albumins

Globulins

The table shows that demodicosis is accompanied by hyperprotsinemia and hyperglobulinemia. Hyperglobulinsmia is explained by an increase in the concentration of IgG, while the amount of IgM remains practically unchanged.

The study of the immune status of dogs using the reaction of phytohemagglutinin (PHA) set the task of the study:

Confirm the hypothesis that demodicosis is a manifestation of immunodeficiency;
to study the restorative ability of T-lymphocyte mitosis during the treatment of demodicosis;
to determine the significance of this test in order to predict demodicosis.
In the first series of experiments, 4 groups of dogs with 7 heads each were used. Group 1 - American Cocker Spanis puppies 10-12 weeks of age: Group 2 - adult dogs of this breed; Group 3 - puppies 10-12 months of age of different breeds, Group 4 - adult dogs of different breeds.

Phytohemagglutinin (PHA) was injected intradermally at a dose of 0.1 mm (10 mg) into the skin fold under the arm behind the shoulder, just below the elbow projection zone. The reaction was recorded after 30, 60 minutes, 24, 48 and 72 hours Using a ballpoint pen, the swelling zone was surrounded, then graph paper was applied, pre-moistening it with a swab with alcohol At the same time, the ink transferred to the paper and showed the swelling area in mm2 the maximum response in all cases was 24 hours after PHA injection. The percentage increase in the thickness of the skin folds was as follows: 1 group - 22.9 (2.25%), 2 group - 69.2 (3.18%), 3 group - 57.3 (2.62%), 4 group - 65.6 (7, 7%)

Thus, comparing puppies of the same age, we see that Cocker Spaniels have a deficit in the response to PHA.

In the second series of experiments, 3 groups of dogs, 7 heads each, were used. group 1 - dogs with a localized form of demodicosis, group 2 - clinically healthy dogs; group 3 - clinically healthy dogs, which were intradermally injected with physiological saline solution.

PHA was administered according to the same scheme. In experimental and control animals, the immediate hypersensitivity response (erythema and swelling) developed after 10-30 minutes. after injection and reached maximum values ​​after 1-2 hours. The saline injection did not cause any reactions.

A late response was obtained at 24 and 48 hours. As a result, it was found that the intensity of erythema and swelling were maximum after 24 hours. The results are presented in table.6.

Table 6 Dog skin response to phytohemagglutinin administration

Reaction time

Control n=7

Demodicosis n=7

% positively responding to the introduction of PHA

Swelling diameter, mm

% positively reacting ma introduction of PHA

Swelling diameter, mm

After 24 hours

After 48 hours

Note: P< 0,05

Thus, phytohemagglutinin promotes the release of histamine from mast cells and multinuclear basophils. This release is accompanied by the presence of IgE immunoglobulins.

Decreased response to the introduction of phytohemagglutinin in dogs with demodicosis indicated cellular immunodeficiency and did not stop until they recovered.

This test, in combination with clinical observation, was later used as a prognosis of the disease.

In the third series of experiments, 5 groups of dogs were used - 4 experimental and 1 control.

The results of the studies showed that in control dogs. (group 1, n=8) erythema was observed in 62.5% of cases. The area of ​​swelling at the injection site of PHA averaged 112.6±19.8 mm2.

In the second group (7 healthy dogs were treated with demizone in therapeutic doses), erythema was observed in 57.1% of cases. The area of ​​edema at the injection site of PHA was 99.3 ± 8.2 mm2, therefore demizone does not affect the mitosis of T-lymphocytes

In dogs of the third group (local scaly form of demodicosis) before the administration of PHA, the swelling area was 51.3±16.4 mm2. Erythema was not noted. At the end of treatment, the swelling area averaged 105.4±18.5 mm2, that is, it increased significantly.

In the fourth group (scaly generalized form), before treatment, the area of ​​swelling at the injection site of PHA was 8.5 ± 3.5 mm2, i.e., cellular reactivity was negligible. Erythema was not observed. Obviously, with an increase in the number of ticks, the depression of T-lymphocytes increased. During treatment, reactivity averaged 58.5*11.4 mm2. 5 out of 8 dogs developed erythema (62.5%).

In generalized pyodemodecosis (group 5), reactivity tests were performed in 11 dogs. The average edema area was 22±8.3 mm2. Erythema was noted in 4 (36.6%) dogs. Obviously, with purulent processes in the skin, there are no obstacles for the reproduction of lymphocytes and macrophages.

In the course of treatment, the swelling area increased to an average of 63.4±8.2 mm2 Erythema was noted in 7 dogs (63 6%). At the end of treatment, the swelling area was 132.5±20.6 mm2. Erythema was present in 9 dogs (81.8%).

In 2 dogs (1 Cocker Spaniel and 1 Staffordshire Terrier) without clinical improvement, the reaction surface decreased and remained at a low level - 11.3±2.1 mm2 - for 4 months (observation period)

Thus, the results of the experiments showed that the intradermal PHA reaction is read already after 30 minutes. after setting and kept up to 48 hours, and most of the control dogs reacted after this period.

With the scaly localized form of demodicosis, 100% of dogs reacted, while with the scaly generalized form - 20% and with pyodemodecosis - 74%.

It is quite obvious that there is a significant difference between the lymphocytic response of healthy and demodectic dogs. A difference was also found between dogs with different forms of the disease.

At a high intensity of invasion, T-lymphocytes do not multiply and the reaction decreases.

In dogs of the control group, the intradermal PHA reaction causes erythema and swelling with an area of ​​112.61 19.8 mm2. In demodectic dogs, such an injection causes swelling - 51.3 ± 16.4 mm2. During treatment, T-cell inhibition decreased and the reactive surface increased.

In dogs with squamous demodicosis, an increase in reactive area parallels clinical improvement, with one recurrence heralding immunosuppression.

Six of 11 dogs with pyodemodecosis showed clinical improvement, accompanied by an increase in the reactive surface. In all animals, at the end of treatment, the swelling area approached that of the controls. Three cockers at the age of 1 year in this group had pododermatitis, with treatment the swelling area increased from 22.1 mm2 to 63.2 mm2. After 2.5 months, one dog again had severe pododermatitis. with a second course of treatment, the dog's condition improved; the reaction was 61.3 mm2. In one Doberman, despite complete recovery of the skin structure, a negative T-cell reaction led to the conclusion that there was immunosuppression caused by another pathogen.

Thus, the intradermal PHA reaction makes it possible to control the presence of immunosuppression syndrome, as well as to observe immune development during the treatment of demodicosis.

However, it must be borne in mind that when demodicosis is complicated by a bacterial infection, local macrophage activity reveals positive lymphocytic reactivity.

Based on the literature data and our own research, we propose the following scheme of the disease development mechanism in dogs with demodicosis (Scheme 3).

Demodicosis is one of the difficult-to-treat skin diseases of dogs. It is especially difficult to treat generalized pyodemodecosis, since the entire body is involved in the pathological process.

The complexity of chemotherapy lies in the difficult delivery of the active substance to the place of localization of ticks (to the colony) for their complete destruction. Acoricides of systemic action (organophosphorus preparations, ivermectins, some pyrethroids, etc.) kill adults, but the preimaginal stages, which are in a passive state, do not die, since they do not feed. Upon the onset of favorable conditions (cessation of treatments), the larvae and nymphs become active, while the deutonymph molts onto adults, which reproduce, and the number of mites quickly recovers (5, 6).

Treatment of demodicosis should be complex and based on the suppression of the vital activity of Demodex canis mites. In this case, it is necessary to exclude all predisposing factors, avoid the use of corticosteroids, treat secondary pyoderma with systemic antibiotics, do control skin scrapings every 3-4 weeks, continue treatment until 3 negative results are obtained.

For the treatment of dogs with demodicosis, according to the current instructions, the following are used:

1% trypansini solution in physiological saline solution. It is prepared as follows: the required amount of trypansini is added to a hot (80-90 ° C) physiological saline solution, thoroughly filtered and sterilized in a water bath for 30 minutes. from the moment of boiling. The cooled solution is injected intravenously at a dose of 0.5-1.0 ml per 1 kg of body weight.

In our studies, with four times the use of the drug with an interval of 7 days, out of 15 dogs with generalized demodicosis, 11 recovered (extense efficiency - 71.6%). significantly improved, however, after 6-9 months, 4 of them again had lesions and mites at all stages of development. Obviously, the 4 injections of the drug recommended by the instructions are not enough to completely cure the animals.

Of this group of compounds, in our opinion, the drug berenyl from Hoechst, Germany, deserves more attention. The drug is administered subcutaneously in the form of a 7% solution at a dose of 3.5 ml/kg of body weight three times with an interval of 16 days.

Before the administration of the drug, dogs must be prescribed cardiac agents (caffeine, camphor oil, sulfakamphokain, etc.)

The exteno-efficiency of berenyl in generalized pyodemodecosis in our experiments was 91.6%. Only 2 out of 33 dogs (6.06%) relapsed at 7 and 9 months.

According to the literature data, among organophosphorus preparations for demodicosis, chlorophos (trichlorfon, neguvon), sebacyl, ronnel, and saifli are effective (1, 2, 4, 8,11).

A 2% solution of chlorophos is washed every other day with the entire surface of the body until recovery, however, chlorophos does not have a systemic effect and does not penetrate into colonies deep in the skin.

Ronnel is effective when dissolved in propylene glycol (180 ml of 33% Ronnel per 1 liter of propylene glycol). It is applied to the affected area daily until recovery (only 6-9 times). However, when more than 1/3 of the body surface is treated, toxicosis often occurs, which is removed by anticholinergics (atropine sulfate, phospholitin) or cholinesterase reactivators (dipiroxime).

For systemic treatment, hypodermin-chlorophos, hypchlophos and saifli are used.

With a local form of lesion with hypodermin-chlorophos, the affected areas are abundantly moistened, with a generalized one, the drug is applied to the skin of the back along the spinal column, departing from it 2-3 cm, at a dose of 0.15 ml per 1 kg of body weight four times with an interval of 7 days.

Hyphlophos (dematef) is used in the same way as hypodermin-chlorophos at a dose of 0.17 ml per 1 kg of body weight four times with an interval of 7 days.

In our experiments with a local squamous form, its efficiency was 100%.

With generalized pyodemodecosis, the drug at the indicated dose was 81.8% effective, at a dose of 0.2 ml / kg - 100%.

Sayfly (cythioate) is used at the rate of 1 tablet per 10 kg of body weight 2 times a week for 6 weeks.

In the squamous form, soap K is effective. It is used in the form of a 5% aqueous emulsion, abundantly wetting the affected areas, 6-8 times with an interval of 5 days.

At present, synthetic pyrethroids, which have a wide spectrum of acaricidal activity, moderate persistence, and relatively low toxicity to warm-blooded animals, are of great interest. Taking into account the fact that pyrethroids do not have the ability to accumulate in the biosphere and are ecologically low-hazard, they are considered the most promising pesticides [6, 11, 25]. .G

SV Larionov (6) was the first to propose systemically acting pyrethroids in dogs with demodicosis - pedems, cibon, panacid and cydem.

Pedems (based on permethrin) is applied to the lesions at the rate of 1-1.5 ml per 1 kg of body weight twice with an interval of 7 days. The remaining drug (from the total dose) is applied to the skin of the back, having previously parted the hairline by pouring on the sides along the spinal column.

Cydem (based on cypermethrin) in aerosol and propellant-free containers is applied to the dog's skin by pressing the spray head or pump handle from a distance of 5-10 cm from the treated surface, directing the aerosol torch to the affected areas of the body at a dose of 1 g per 1 kg of body weight. Processing is carried out four times with an interval of 7 days.

Decis, danitol, baytichol are used in the form of oil solutions in a 0.025% concentration 3-4 times with an interval of 10 days by rubbing into the affected areas of the skin.

In our studies, in the treatment of 48 dogs of various breeds and varying degrees of damage by D. canis ticks, including 29 with generalized demodicosis, 100% efficiency was obtained with the use of demizone (deltamethrin). The drug was applied to the lesions twice with an interval of 7 days, abundantly wetting the skin of the bald zone and border areas of the skin 0.5-1 cm wide at a dose of 0.5-1.0 ml/kg of body weight.

Of the other systemically acting pyrethroids, we have obtained good results with miatrin-C (pour on). It is a light yellow transparent liquid with a specific odor. Miatrin-C in the local squamous form was applied to the lesions at a dose of 0.5 ml per 1 kg of body weight. In the case when the area of ​​the affected areas is small, the remains of miatrin-C were applied again, after 15 minutes; The drug remaining after re-treatment (from the total dose), having previously parted the hairline, is applied to the skin of the back (by watering), along the sides along the spinal column, 2-3 si away from it. All of the 54 dogs recovered after four times the use of miatrin-C (extensity efficiency - 100%).

Benzyl benzoate is used as a 20% ointment. It is applied to the skin of the affected area and border areas of the healthy area 1.0 cm wide using a swab of foam sponge in the amount of 0.3 g/cm 17-8 times with an interval of 5 days.

In mammals, GABA is an inhibitory neurotransmitter found only in the central nervous system, while in arthropods it controls peripheral musculature. In mammals, ivermechtin does not readily cross the blood-brain barrier and has a wide margin of safety. However, in some breeds of dogs (collie, bobtail, sheltie, etc.), ivermectin is able to overcome the blood-brain barrier and cause toxicosis. Increased sensitivity to ivermectin is noted in young animals, which is explained by the permeability of the blood-brain barrier at this age (29).

Ivomek, like almost all newly created acaricides, was tested in dogs with demodicosis. So, K. Pawlowski reports that in case of squamous form of demodicosis in dogs, cure can be achieved by subcutaneous injections of ivomec at a dose of 250 μg of ivermectin per 1 kg of body weight with an interval of 6-7 days. The author notes that recovery occurs after 2-6 injections.

G. Khristov and I. Mikhailov, having tested Ivomec on 12 dogs of hunting breeds, note that two subcutaneous injections of Ivomec at a dose of 200 μg of ivermectin with an interval of 20 days are sufficient to completely cure dogs from demodicosis.

However, S.V. Larionov (6) failed to cure demodicosis in dogs with severe pustular form when using ivomec at a dose of 350 µg/kg with repeated use.

Our studies on 73 dogs confirm the opinion of S.V. Larionov. After 2-3 injections of various doses of the drug, there is a significant improvement in the general condition of the dogs, hair begins to grow, clinical signs of the disease disappear, but after 6-8 months. in 78% of cases, we observed relapses of the disease.

We believe that the use of ivsrmectin preparations for the treatment of canine demodicosis is problematic, since they are not licensed for this type of animal and have significant adverse reactions.

The toxicity of ivomec is manifested by subcutaneous administration in the form of a local pain reaction, local inflammatory edema at the injection site, as well as a violation of the functional state of the liver.

Quincke's edema can develop in dogs with the subcutaneous injection of cidectin (1% moxidectin solution) from Cyanamide.

Noteworthy is a complex method for the treatment of generalized demodicosis, including subcutaneous administration of ivomec, external application of sulfur-tar liniment, and feeding of alimentary sulfur (5,6). Ivomek is administered subcutaneously to dogs twice: on the first day - at a dose of 0.2 ml per 10 kg of body weight, on the 7th day - 0.3 ml per 10 kg of body weight. Sulfur-tar liniment is applied to the affected areas for 30 days, consisting of 1 part of birch tar, 2 parts of sulfur and 5 parts of tetravit (trivit) - the first week - daily, and then 1 time in 5 days. At the same time, alimentary sulfur (GOST 127-76) is fed once daily at a dose of 0.5 g per 10 kg of body weight for 30 days.

We propose instead of sulfur-tar linimeite in this scheme to use Vaganov's ointment, consisting of ASD-3 - 100.0; sulfur - 100.0; birch tar - 20.0; lysol - 30.0. vaseline - 800.0. Its composition is selected in such a way that, having a detrimental effect on D.canis ticks, it has a positive effect on the affected skin and thus on the body of dogs (antimicrobial, anti-inflammatory, keratolytic effect, etc.). In addition, the components of the ointment are available, inexpensive and harmless to animals.

The advantages of the method include the absence of recurrence of the disease and the reduction of the course of treatment for demodicosis to 30 days.

Of the acaricidal drugs that are highly effective in the treatment of generalized demodicosis, one can name amitraz. It belongs to the group of formamidines and is a monoamine oxidase inhibitor, it successfully acts on ticks resistant to aosenids, organochlorine and phosphorus insecticides. The effect of the drug is manifested already in the first hours after the start of treatment. The use of amitraz every 10 days breaks the life cycle of ticks, which allows you to take control of the development of invasion. The residual effect is 7-9 days depending on the climate. Amitraz is rapidly degraded in soil and does not pollute the environment.

Firm "Upjohn" produces amitraz in the form of a liquid concentrate called mitaban, "Pitman Moore" - called triatrix, triatox. The working solution is prepared according to the instructions and used to obtain a double negative microscopy result. Amitraz can cause transient insomnia, in addition, animals should be protected from stressful effects for 24 hours after the use of the drug.

In St. Petersburg, the drug amitrazine is produced in the form of a ready-to-use 0.25% solution of amitraz on dimexide. It gives a good effect in the treatment of generalized and local forms of demodicosis.

The French company "Biokanin" produces collars for dogs containing amitraz. This collar is replaced once a month. The course of treatment is 3-4 months.

We have noted the high efficiency of 0.03% aqueous emulsion of amitraz with five applications with an interval of 7 days (92.3%).

For the treatment of generalized demodicosis with amitraz, the following recommendations must be observed:

Do not use concentrations of amitraz above 0.05%.
The interval between treatments should not exceed 10 days.
Fully trim long haired dogs.
Prepare an aqueous emulsion on the day of use.
Before using the drug, the dog is washed with keratolytic zoo shampoos (sulfur-salicylic, shampoo containing benzoyl peroxide, etc.).
Rub the solution into the skin with a sponge.
Do not rinse.
Apply air dry.
Do not allow the dog to remain wet between applications of Amitraz.
Carry out treatment in a well-ventilated room.
Observe personal safety measures.
Despite the fact that a significant number of acharicidal preparations of various chemical groups have been proposed for the treatment of dogs, in our opinion, amitraz deserves the most attention. According to a number of authors, this drug has high therapeutic efficacy, low toxicity, is well tolerated by animals at recommended doses, has no side effects and complications, does not have skin-resorptive and long-term toxic effects, which makes amitraz and preparations based on it very promising agents. treatment of demodicosis in dogs.

We also believe that the effectiveness of amitraz in the treatment of generalized demodicosis is much higher when it is used in combination with immunomodulators.

The auricles of dogs are treated with aerosols of acrodex, dermatosol, cyodrin, psorotol, perod or acrosol from a distance of 10 cm by pressing the valve of the aerosol can for 1-2 seconds.

Along with the use of specific drugs, dogs are prescribed vitamins according to Ryss, pushnovit, gendevit, etc.

The effectiveness of the treatment is checked after 25, 30 and 45 days. At the same time, skin scrapings are necessarily made and an acarogram is taken.

PREVENTION

Some authors have shown the possibility of preventing this disease in newborn puppies by treating cervical bitches with ivomec at a dose of 200 µg/kg. Processing is carried out six to seven days before whelping. Puppies should be weaned no later than 28 days of age (1,2,6).

Noteworthy is the use of akaficidal collars, both domestic and foreign, for the prevention of demodicosis.

In our experiments, six cervical bitches with scaly form of demodicosis were put on "Artemon" collars based on deyatamethrin 20 days before whelping, four other infected animals served as controls. In the experimental and control groups, puppies were observed for 2 years. As a result, it was found that out of 31 puppies, obtained from bitches, which were put on collars "Artemon", two (6.5%) fell ill with demodicosis; in the second of 27 - 10 (37.3%).

Mandatory elements in the prevention of demodicosis in dogs are:

Quarterly clinical examination;
in kennels - the acquisition of dogs in groups should be carried out only after a month of quarantine and preventive treatment;
during the period of natural molting, introduce sulfur into the diet;
organize the feeding of dogs on a strict diet; animals must be carefully examined before mating; even with a slight defeat by demodicosis, animals should not be allowed to mate; once a month, the resting places of dogs must be subjected to desacarization with hot (50-60 °) water.
Prevention may include limiting contact with an obviously sick animal, as well as taking measures to prevent the occurrence of non-communicable skin diseases.1