Case history: Demodicosis in dogs. Case history of a dog successfully treated for demodicosis (difficult case)

Pathogen. The disease is caused by a tick Demodex canis(demo-dex canine) family Demodecidae suborder Trombidiformes. Sexual dimorphism in ticks E. satB clearly expressed in the imago phase. The male is larger than the female, and the male has a much shorter opisthosoma. When differentiating males from females, body shape should also be taken into account. If the female has a generally worm-like body shape, then the male clearly has a more voluminous middle part - the podosome. In the male, at the place of transition of the podosoma to the opisthosoma, the constriction of the body is clearly expressed.

The Demodex egg is spindle-shaped (flask-shaped), covered with a delicate, transparent shell. The anterior pole of the egg is rounded, while the posterior pole is sharper and somewhat elongated.

Developmental biology. Under favorable conditions, the development cycle occurs within 25-30 days, in the warm period - 14-15 days. During this time, the tick goes through five developmental phases: egg, larva, first nymph (protonymph), second nymph (deutonymph) and adult. Ticks isolated from the host remain viable at room temperature in dry air for no more than 5 days, and on the skin of dogs for up to 7 days.

In a humid environment, especially in crusts and scabs at a temperature of 16...20°C, mites survive for 2-3 weeks.

Demodicosis is a typical disease of young dogs (dogs aged 6 months to 2 years are most seriously ill).

The development of the disease is facilitated by weakened immunity, endocrine diseases, concomitant diseases (helminthiasis, entomosis, sarcoptic mange, etc.), chemotherapy, autoimmune diseases, pregnancy, lactation, poor skin hygiene (frequent washing, causing skin irritation, keeping dogs in a damp room).

The disease is more common in short-haired dogs of the Rottweiler, Doberman Pinscher, German Shepherd, Bull Terrier and Pit Bull Terrier, Great Dane, Shorthaired Pointer, and Drathaar breeds. Much less frequently, the causative agent of demodicosis is found in dogs of such breeds as Pekingese, Charley, Newfoundland, Chow Chow, Mastino Neapolitan.

There is a breed predisposition to the disease (Scottish Terrier, Shar Pei, Afghan Hound, Great Dane, English Bulldog, West Highland White Terrier, Doberman), and mongrel dogs and mixed breeds are less susceptible to this disease. Since the juvenile generalized form of demodicosis is hereditary, a family predisposition can also be traced.

Dogs with low and average body condition are most susceptible to the disease, and dogs with above average body condition are less likely to become infected.

The peak of the disease is observed in the winter-spring period, which is associated with a decrease in the general resistance of the animal’s body and a decrease in skin tone due to lack of insolation.

The disease is low contagious. Infection occurs only by contact and only by sexually mature forms of the mite, which migrate from the follicles to the surface of the skin and actively move along it. Environmental contamination does not matter. Currently, most authors are inclined to believe that the contact route of transmission of the pathogen from a sick mother to a newborn is the main, if not the only one.

Infection occurs through contact with sick animals during group keeping and mating, or through contact with objects (cages, houses, equipment) that were used to keep sick dogs. Nursery staff can mechanically transmit demodicosis pathogens. In addition, dogs become infected with demodicosis when hunting predatory animals (foxes, arctic foxes, wolves). Puppies are susceptible to infection with demodicosis from the first days of life.

Symptoms of the disease. More often, the disease takes a chronic form, and with complications, the symptoms accompanying the underlying disease can develop quite quickly.

Based on the area of damage to the body of dogs, localized and generalized forms of demodicosis are distinguished.

Based on the localization of the demodicosis process, pododemodicosis (paw demodicosis) and otodemodecosis (ear demodicosis) are distinguished.

According to the nature of the lesion, focal (scaly, squamous), nodular (papular), pustular and mixed forms are distinguished.

Juvenile demodicosis, observed in dogs under the age of one year, is classified as a separate nosoform.

Sometimes an asymptomatic form of infection is also observed.

Papular (nodular) the form is characterized by the formation of papules on the skin, most often in the area of the head, back and root of the tail, ranging in size from 1 to 7 mm in diameter, with a very dense consistency. Hair is preserved on the surface of large papules.

Pustular form (pyodemodecosis) characterized by the formation of pustules with a diameter of 1-4 mm on the skin. Subsequently, they open and their contents flow out. Hyperemia occurs, cracks in the skin appear, which becomes thick, moist, folded and acquires an intense red color, especially between the folds. Hair in the affected areas is sparse. As a result of a secondary infection, pyoderma occurs with the formation of ulcers.

Mixed form- the most severe and widespread. It is characterized by necrosis of the epidermis and its desquamation. Ulcers often form in place of the opened pustules. Hair falls out, and in balding areas the skin becomes very wrinkled, giving it a “corrugated” appearance. Due to a violation of thermoregulation, the dog experiences chills even in a warm room. Infestation often ends in death.

Generalized form the disease develops rapidly. Extensive lesions appear on the skin. The inflammatory process penetrates deeply into the tissues, even involving internal organs, which leads to general intoxication of the dog’s body.

Asymptomatic form The disease occurs in adult dogs. There are no characteristic signs of the disease. In this form, demodexes are found in the skin of dogs, completely unchanged in appearance.

Pododemodicosis (demodectic nododermatitis, demodicosis of paws). Localization of Demodex in the paw area is most often found in dogs with a generalized form of the disease. The course of invasion can be complicated by secondary bacterial infections. Old English Sheepdogs, Shar-Peis, and Cocker Spaniels are predisposed to this form of invasion. To detect mites and make a differential diagnosis, a biopsy is sometimes required due to the deeper localization of demodexes.

Diagnosis. The diagnosis is made on the basis of epizootological data, symptoms of the disease and the results of an acarological study of animal skin scrapings or the contents of demodectic nodules.

Make deep (until ichor or drops of blood appear) skin scrapings from 2-3 affected areas of the dog’s body (especially in the area of the head and paws). In this case, the skin should be squeezed from the sides with your fingers so that the mites come out of the hair follicle.

To confirm the diagnosis, it is necessary to perform an acarogram (counting eggs, larvae, nymphs and adults), since single mites can be detected in skin scrapings from clinically healthy dogs.

With a localized form of demodicosis, you can additionally take scrapings from healthy skin, since a large number of mites found may indicate the danger of subsequent generalization of the disease.

Demodicosis is differentiated from diseases with similar symptoms: sarcoptic mange, otodectosis, cheyletiellosis, aphanipterosis, trichophytosis microsporia, allergies, pyoderma of bacterial origin, etc.

Treatment. If there are signs of demodicosis in a dog, the form of manifestation of the invasion should be determined, since the treatment and prognosis of the disease are different in each case.

Treatment of demodicosis should be comprehensive and based on suppressing the vital activity of mites, normalizing skin function, improving hair growth, etc. Therefore, in addition to insecticides, it is necessary to use immunocorrective therapy, vitamins, and hepatoprotectors. In case of a complicated form, specific treatment is carried out - antifungal, antimicrobial, etc.

For treatment, insecticides based on pyretrodes, fi-pronil, imidacloprid in the form of ointments, gels, emulsions, solutions, aerosols, as well as preparations from the group of macrocyclic lactones (injection forms, ointments, gels) are used. The following drugs are used: advocate, ivermek gel, ivermek spray, amidel-gel, aversectin ointment, amit forte, amit, amitan, acaromectin, dermatol, tsidem, tsipam, entomozan super, epacid-alpha, Bars spot-on, etc.

Prevention. Kennels and clubs must be staffed with healthy dogs. Do not allow dogs that have had demodicosis to be bred. Producers whose offspring include puppies affected by demodicosis are also not allowed to reproduce.

A good way to prevent demodicosis in dogs is to use collars with insecticides.

The most important thing with this disease is to immediately begin treatment at the first symptoms. If you do not comply with the deadlines, then the disease will develop into a chronic disease, which you will have great difficulty in getting rid of.

At the same time, demodex mites cause severe damage to people’s appearance, which causes serious complexes, depression, and low self-esteem. For such a serious disease as eye demodicosis, treatment takes about 4 months, it all depends on the severity of the disease and the type of demodex mites.

The main thing is not to stop treatment at the first improvements, but they will come already in the first weeks of treatment. When a severe stage of demodicosis of the eyelids occurs, treatment will last about six months.

If a person refuses to carry out timely and correct treatment, the disease begins to progress, leading to hair loss, strong growth of nasal tissue, inflammation of the cornea and other affected parts of the body.

The principle of treating such a disease is to identify the main cause that provoked the disease. It is extremely important that the patient goes on a special diet and definitely excludes all alcoholic drinks, tobacco, spicy foods, and caffeine.

Personal hygiene should become the main companion of life: constantly change towels and bed linen, avoid places with hot air. “After diagnosis, along with treatment of identified chronic diseases, it is necessary to lead a healthy lifestyle, first of all, alternating physical activity with rest, especially when working at the computer, doing morning exercises, and monitoring your diet.

Walking in the fresh air for at least 1 hour every day is mandatory,” this is what ophthalmologist of the highest category, Doctor of Medical Sciences L.P. advises

Volkova. You should definitely avoid self-medication completely, as this can lead to serious consequences.

If you want to use folk remedies, you must first consult your doctor.

Medications for illness

When treating such a serious illness, local ointments are ideal. Demelan - external ointment for the eyelids is used for demodicosis.

Before using it, first remove dry crusts from the eyelashes and treat the eyelid with an alcohol solution of calendula. Then apply the ointment, gently massaging the eyelid.

It must be used twice a day for at least one and a half months. Another ointment, Blefarogel, will help cure demodicosis.

It is also necessary to treat the eyelids of all family members for prevention. Trichosexual ointment is allowed to be used during pregnancy and breastfeeding.

To relieve severe itching, it is necessary to drop Acular or Dexamethasone drops into the eyes.

Folk remedies for demodicosis of the eyes

This type of treatment should only be carried out with medication. It won't help on its own.

But before using any product, be sure to consult your doctor. A decoction of wormwood, which is taken orally to kill ticks, is perfect.

You need to know that tansy is poisonous, so follow the dosage exactly. You need to treat your eyes with the infusion, instill them three times a day.

You can make an ointment from the plant. The eyelid treated with alcohol should be smeared with the resulting product for half an hour.

Be sure to use massage during treatment. It is extremely important for complex treatment.

Demodicosis is a serious disease that must be treated when the first symptoms appear. Be sure to consult a doctor for a full examination, a clear analysis, and the appointment of competent treatment.

Students, graduate students, young scientists who use the knowledge base in their studies and work will be very grateful to you.

Posted on http://allbest.ru

Department for Personnel Policy and Education of the Russian Federation

Federal State Educational Institution of Higher Professional Education “Krasnoyarsk State Agrarian University”

Department of Epizootology, Microbiology and Veterinary and Sanitary Expertise

Coursework

Demodectic mange in dogs

Completed: art. IV course,

Checked by: Ave. Shcherbak O.I.

Krasnoyarsk - 2004

Introduction

1.3 Biology of ticks

1.4 Pathogenesis of demodicosis

1.5 Diagnosis of demodicosis

Introduction

The causative agent of the disease is thrombidiform mites; their description was first made 120 years ago. However, many questions of morphobiology, pathogenesis and specificity have not been resolved and remain controversial to this day.

This, in turn, leads to incorrect diagnosis and treatment of demodicosis.

1. Brief information about the disease and characteristics of the causative agent of demodicosis

Demodectic mange - a widespread chronic seasonal disease that manifests itself as focal skin lesions as a result of the settlement of Demodex mites in the hair follicles and sebaceous glands of animals.

1.1 History of the study of demodicosis

Many scientists have studied the morphology of pathogens, taxonomy, biology, diagnosis and treatment of the disease. The first mention of mites of the genus Demodex dates back to 1841, when Berger discovered them in human acne. Later, T. Tulk (1844) and P. Megnin (1877) reported the presence of such mites in dogs. In Russia, the first mentions of ticks of this genus in dogs and cattle appeared in 1845. According to many scientists, the causative agents of demodectic infestation are strictly specific to the host species.

Significant research on the problem of demodicosis in carnivores has been and is currently being carried out by many scientists. Among them is Yu.S. Balashov, S.V. Larionov, F.I. Vasilevich, M.V. Rozovenko, O.A. Raga, L.N. Skosyrskikh, B.A. Frolov, J. Stamm, D.K. Polyakov, L.Kh. Azamatov, R.O. Drummond, W.F. Fisher.

1.2 Systematics and morphology of mites

Today, the following systematic position of mites is accepted (O"Connor, 1982):

Type: Arthropoda

P/type: Chelicerata

Class: Arachnida

Squad: Acariformes, Zoch.

P/squad: Trombidiformes, Reuter

N/family: Demodecoides, Bauns

Family: Demodicidae, Nik

Genus: Demodex

The most common types:

The female has a cigar-shaped body, 0.19 - 0.22 microns long. The gnathosoma is wide, protruding forward, and on the dorsal side it shows the main, second and terminal segments of the palp and paired seta of the palp.

On the ventral side, on the terminal segments of the palps on both sides there are six very short papillae in the form of a cone. Further between the pulps there are thin stylet-shaped chelicerae. They are enclosed in a case. At their base, a mouth opening is visible, and just below it there are paired respiratory openings. On the dorsal surface there is a propodosomal shield with rounded corners. Along its periphery there are 4 microchaete bristles. The opisthosoma is significantly longer than the anterior part of the body, with transverse annular folds.

Figure 1. Demodex canis: A- from the ventral side; B- from the dorsal side

On the ventral side, 4 pairs of short cone-shaped legs with 5 movable segments are visible on the propodosome. There are 2 claws on the paws of all legs. Along the midline of the body there are two rows of coxal areas. At the level of the 4th pair of legs, between them there is a genital opening in the form of a longitudinal slit.

Ticks have weakly expressed sexual dimorphism. Unlike females, males have a body length of 0.16 - 0.18 microns, a narrower opisthosoma. The reproductive apparatus is located on the dorsal side at the level of the 2nd and 3rd pairs of legs.

1.3 Biology of ticks

Ticks D. Withanis In their development, they pass through the phases of egg, larva, protonymph, deutonymph and imago. The duration of the cycle depends on the season of the year, the general condition of the animal (especially the skin), living conditions and feeding.

Moreover, the transition from one phase to another occurs through a complex process of restructuring the body: histolysis - destruction of organs and histogenesis - formation of organs of a new individual. In the warm season, the entire cycle occurs in 18 - 20 days, and in autumn and winter 22 - 25 days. Mites develop only in hair follicles and sebaceous glands. Accumulations of ticks in these places were previously called “Kruglikovsky’s balls.” Nowadays they are usually called colonies or papules. Their number on one animal - a dog - can reach up to 200-300, and in cattle - up to 5 million. Females live in papules for up to 10 months, males - 3-5 days. The growth of papules continues for 3 weeks, and when their diameter reaches 10 mm, the “dome” is opened. When mites leave the “old” papules, and these are mostly females, they move around the skin for 2-3 days, looking for suitable follicles. When all individuals leave their home, the cavity will be overgrown with connective tissue or filled with fat of dense consistency.

Demodexes are relatively stable in the external environment. Outside the host’s body they remain viable at 19 0 C, at 18 0 C - 3-4 days, from 1 to 5 0 C - 11-18 days, at -6 -9 0 C - up to 5 days, viability in mineral oil - 4 days. These data are interesting not only from a biological point of view; they are important to take into account when organizing treatment and prevention.

1.4 Pathogenesis of demodicosis

Mites begin to affect the host's body from the moment they penetrate the hair follicles. There they feed on the epithelial cells of the root sheath of the hair follicle, causing its atrophy. When a papule ruptures, focal inflammation forms around it, connective tissue and elastin fibers are destroyed, it wrinkles and becomes tanned. During tick migration, as well as when papules rupture, ticks release toxic metabolic products that cause biochemical changes at the level of the whole organism. It was found that this increases the concentration of carbohydrate components of serum glycoproteins and the level of hexoses associated with protein, which indicates disorganization of the main substance of the subcutaneous connective tissue.

Demodex metabolic products lead to a decrease in the level of diamine oxidase and a slowdown in the processes of collagen synthesis. This sharply reduces the immunobiological reactivity of the host organism.

Foreign scientists studied the immune status of the host organism during tick infestation. At the same time, not only the indicators of natural resistance in dogs change (lysozyme activity, bactericidal activity of blood serum), but also the level of cellular and humoral immunity. However, stable immunity to this disease is not developed. Animals that have recovered from the disease can become infected with demodicosis again after some time. Intrauterine infection has not been established, but the hereditary nature of the disease with a generalized form of demodicosis has been proven.

1.5 Diagnosis of demodicosis

1.5.1 Epizootological data and clinical signs of demodicosis

Demodicosis infestation among dogs is widespread. Similar diseases have been reported in most countries. A total of 22 dog breeds have been identified in which this pathology occurs. Smooth-haired breeds are most susceptible to the disease, and long-haired breeds are collies, shelties, and shepherds. Infection and disease in animals is possible as early as three weeks of age, but most often it occurs at 2 to 3 years of age.

As can be seen from graph I, the greatest peak of invasion is observed in March (70%) and September (60%), i.e. when the active natural change of animal hair begins. Demodicosis is also recorded in the cat population. According to M.V. Shustrova, this pathology is most common in cats of the Russian Blue breed, as well as in animals of the Siamese-Oriental group. Demodicosis in dogs manifests itself in scaly, papular, generalized (chronic), and complicated forms.

Initially, the acute course of the disease in dogs, especially puppies, occurs in a scaly form. At the same time, bald areas with small scales of keratinized gray epidermis appear on the skin around the eyes, nose, and outer surface of the ears, which are easily removed. This period lasts 1 - 1.5 weeks.

Next comes the period of papular manifestations of the disease. Papules appear on the skin in the affected areas (they are called colonies). By the 30th day, they turn into vesicles, inside them there is a thick, paste-like mass of gray color, their diameter is 7-10 microns. At 4-5 weeks from the onset of the disease, the vesicles burst, and a brown scab forms in these places. During this period, dogs' appetite sharply deteriorates and weight loss occurs. With complete absence of treatment, as well as with improper feeding, the disease becomes generalized. In this case, the signs of two forms appear simultaneously. After two months, the animals become exhausted, they become timid, and are reluctant to go for walks. If the dog does not have concomitant pathologies, then the process becomes chronic. Clinical signs may be smoothed out.

General condition may improve. However, after 1 - 2 weeks, relapses of the disease occur, with the appearance of new extensive bald areas of skin covered with a thick, bumpy crust, and an ichorous odor emanates from the dogs. Such a clinical picture can be observed for several years, but in the end the animal dies. Throughout this period, the sick dog is a constant source of infection for other dogs.

If owners continue to feed incorrectly, neglect the rules of care and maintenance, and do not provide qualified treatment, demodicosis becomes complicated. Secondary microflora - staphylococci and fungi of the genus Candida. During this period of the disease, when most of the follicles suitable for tick life are affected, demodexes migrate to the internal organs: liver, kidneys, spleen, etc.

1.5.2 Laboratory tests

The diagnosis is made comprehensively, taking into account the epizootology, pathogenesis and clinical picture of the disease.

The diagnosis is confirmed in only one way - by taking a scraping.

To do this, make a deep scraping or incision of the affected area of the skin, the contents of which are immediately placed in a drop of a preservative (50% glycerin or 10% NaOH, any oil, kerosene). To prepare permanent micropreparations, mites are poured into a gum arabic mixture of Fora - Berlese.

After taking a scraping, the animal should treat the wound so that secondary microflora does not get there.

If an animal has a generalized or complicated form of the disease, then its fecal masses can be examined by any flotation method (Darling, Fulleborn, Kotelnikov). D.canis mites will be found in the smears, most often dead.

When viewing preparations under a microscope, one should not only establish the presence of mites, but also determine which phases of development predominate, estimate the number of pathogens and draw a conclusion about the duration of the disease. These data are also important for developing a treatment strategy when choosing an acaricide and determining the frequency of its use.

1.5.3 Establishing a differential diagnosis

It is important to note that there are many diseases of various etiologies, the clinical signs of which are very similar to those of demodicosis. The most important among them are the following:

Sarcoptic mange is a chronic disease of dogs caused by the sarcoptes mite Sarcoptes scabiei var. canis. Small blisters appear where mites enter the skin. The favorite localization of ticks is the skin of the ears, muzzle, elbows, and the root of the tail. The main symptom of the disease is itching.

Cheyletiellosis is caused by thrombidiform mite of the genus Cheyletiella. Lesions on the skin in the form of dandruff along the entire length of the back.

Siphunculatosis is a lice caused by insects of the genus Linognathus. This is a very rare disease that occurs under unsatisfactory living conditions - in damp rooms and with inadequate feeding. Locations: on the head near the ears, along the spine, on the neck. It is characterized by scratching and skin irritation, and severe restlessness of animals at night.

Lice beetles are pathogenic insects of the genera Trichodectes and Heterodoxus. In infested animals, lice eaters are located on the head, paws, and root of the tail. In these areas there is severe constant itching, scratching, hair loss, and severe emaciation of animals.

Trichophytosis is an infectious disease caused by fungi of the genus Trichophyton. Sharply limited flaky areas appear on the skin, the hair is broken off at the base. Inflammation develops in the affected areas with the release of serous-purulent exudate.

Microsporia is an infectious disease caused by fungi of the genus Microsporum. Skin lesions on the face, body, tail. The spots range from 0.5 to 10 - 15 cm in diameter, the affected areas are covered with grayish-white crusts, skin inflammation is mild.

Cold dermatitis usually occurs only in smooth-haired dogs. Dandruff, slight peeling of the skin, and brittle hair appear on the skin of the paws, face, and sides. Within a week the signs disappear.

True food allergy is an immunobiological disease of dogs of all breeds. Food allergy specialist Dr. Richard G. Harvey (UK) points out that most often the skin pathology in this case comes down to itching and scratching, does not depend on the season, and is difficult to treat.

The etiological factors of true food allergies are the intake of foods containing high molecular weight proteins, long polysaccharide chains, as well as their complexes (glycoproteins). These substances are found in various products (milk, beef, horse meat, soy, etc.).

Clinical signs often manifest themselves in the form of a violation of the integrity of the skin, the appearance of bald areas on it in different parts of the body. It has been proven that the disease is of an individual sensitivity nature, so a more precise diagnosis is made taking into account the results of a nutritional test, which uses diets with a limited number of components.

Nutritional imbalances are insufficient or excessive intake of nutrients from the diet. The use of homemade food, which is dominated by boiled cereals, pasta and other components that are not typical for dogs’ digestion, leads to the development of nutritional deficiencies.

2. Organization of treatment and preventive measures

Before you start treating a sick animal, make sure that the diagnosis is correct; determine the cause of this invasion, determine whether the animal is fed and kept correctly, what treatment has already been used.

Treatment of any disease is carried out comprehensively. In the case of demodicosis, the veterinarian has two main methods at his disposal: pharmacotherapy and diet therapy.

Modern science offers many new insectoacaricides of different chemical groups. Multicomponent integrated tick control systems have been created; all that remains is to select the means (see Table I) and determine the regulations for their use. This is done individually for each animal.

Table 1. Main groups of pharmacological drugs for the treatment of animals with demodicosis

Organophosphorus agents used in the form of aqueous emulsions or oil solutions in concentrations of 0.5 - 2% no more. At the same time, at least 3 - 4 treatments are done, once every 7 - 10 days. It should be remembered that all these drugs are toxic to animals and humans, because sharply reduce the level of blood cholinesterase, which ultimately affects processes in the body.

Pyrethroids- analogues of natural pyrethrum compounds, which are used in the form of oil solutions and aqueous emulsions for demodicosis of dogs - 0.05 - 0.075%. The number of treatments is 3 - 4, the interval between them is 5 - 6 days.

Formamedine compounds, primarily amitraz, is used in a 0.02% concentration of an aqueous solution. This drug is effective only for mild lesions (scaly form of invasion).

From the pharmacological group biologically active substances use drugs from the covermectin group. It is rational to use these drugs only in the initial stages of the disease. The drugs are immunosuppressants. They must be used strictly according to the instructions - at least 2 injections every 10 days.

A good effect is achieved by the simultaneous use of ivomec and pyrethroids, especially in chronic cases.

All oil solutions and aqueous emulsions of drugs are applied by rubbing. Methods of watering, bathing and spraying for demodicosis in dogs are not effective!

The most difficult thing is to treat animals with complicated and generalized forms, since it is necessary to destroy the mite, secondary microflora and restore the affected skin and coat in a short period of time.

It is difficult to assess the effects of this drug on the animal body, because it has immunostimulating and antiseptic properties. When introduced into the body, it helps to increase the activity of adenylate cyclase by 1.5-2 times. Marasad retains its acaricidal, bactericidal, and stimulating properties in the skin for 56 days. Two treatments for the complicated form and one for the scaly form are enough for the animal to be cured, the coat and all affected layers of skin are completely restored.

The method of treatment with this remedy is protected by a patent of the Russian Federation. Technical documentation (TU) was prepared for it, and in 1994, the Department of Veterinary Medicine of the Ministry of Agriculture and Food of the Russian Federation approved instructions for its use.

In parallel with drug treatment, it is necessary to organize proper feeding, care and maintenance of animals. This can only be determined and recommended by a qualified specialist.

Considering the fact that demodectic lesions are recorded mainly on the outer integument, and the disease itself is of an immunobiological nature, the use of anti-allergic food is indicated for dietary therapy. The pet owner can create a “homemade” diet, but may use a commercial diet.

In the case of prescribing a “homemade” diet, it is advisable to prepare the following diet: rice (buckwheat) + heart - boil for 3 - 5 minutes, then add vegetable mixtures of cabbage, pumpkin, zucchini, fresh vegetables and herbs + sunflower oil.

We recommend dietary therapy with the Waltham Sensitivity Control Diet (Appendix II) for dogs, developed by specialists at the Waltham Center. This diet shows high effectiveness in treating skin pathologies of various origins (all kinds of allergies, fungal infections, idiosyncrasies), and, of course, in the treatment of demodicosis. The high effectiveness of the diet is due to the presence of exclusively hypoallergenic proteins and carbohydrates in its composition.

The ingredients of this diet are chicken “white” meat, rice, polysaccharides of plant origin, mineral and vitamin complex and water. The biochemical composition of the diet and the dose of its use are indicated in Appendix II. There are no contraindications to the use of this diet. The duration of diet therapy is at least 21 days, and in difficult cases - until the dog is completely cured.

The form of release of the diet is canned food (wet food), packaged in 420 g cans. Countries producing the diet are Austria or Australia.

Preventive measures against demodicosis come down to proper and timely care of the dog, namely its coat, especially during its coat change (March, September).

Dog owners need to regularly contact veterinary specialists for clinical examination of animals with palpation of characteristic areas of demodicosis foci. Sick dogs are isolated and treated.

In addition to destroying ticks on the dog’s body, the premises, materials and care items with which it has come into contact are sprayed or wiped with Bolfo preparations, a 0.1% aqueous solution of chlorophos, dichlorvos, carbosol and other insecticides. At the same time, they improve the conditions of keeping and feeding the animal, and include vitamin and mineral supplements in the diet. It has been found that if a dog’s body develops a deficiency of nutrients such as zinc, sulfur-containing amino acids, and unsaturated fatty acids, this leads to a disruption of general metabolism, and ultimately to changes in the skin. Alopecia appears on the skin in different parts of the body, hair falls out, and itching occurs.

Resistance is increased by regular hardening of puppies and adult dogs.

Owners of dogs that are hereditarily susceptible to the generalized form of demodicosis are strongly advised to sterilize them, or to refrain from producing offspring from diseased lines.

List of used literature

1. Shustrova M.I. Demodectic mange in dogs. - St. Petersburg, 2001. - 30 p.

2. E. Benzior, D.N. Carlotti. Guide to demodicosis in dogs.//Veterinarian - 2000 - No. 3 - P. 32-36.

3. Shustrova M.I. Scabies and demodicosis of animals of various species // Abstract. dis... doc. vet. Sci. - St. Petersburg, 1996. - 40 p.

4. V.I. Romensky, A.A. Shinkarenko, Yu.F. Petrova, A.Yu. Gudkova Pathogenesis of demodicosis in dogs. // Veterinary Medicine - 2003. - No. 11 - pp. 30-31.

5. Starchenkov S.V., Vasilevich F.I. Diseases of small animals: diagnosis, treatment, prevention. - St. Petersburg: Lan, 1999. - P. 475-485.

6. Avdienko V.A. Treatment of dogs with staphylococcal infections and demodicosis complicated by staphylococcosis. // Veterinary medicine - 2003. - No. 7

7. Bratyukha S.P., Nagorny I.S. Diseases of your pets: dogs, cats, songbirds, guinea pigs, aquarium fish. - Kyiv: SME “Alterizis”, 1995. - 335 p.

8. Berghof P.K. Small pets. Diseases and treatment. - M.: Aquarium, 1999. - 307 p.

9. A.D. Belov. Dog diseases. - 2nd edition, erased. - M.: Kolos, 1995 - 307 p.

10. Matveev L.V. Diseases of dogs and cats. - N. Novgorod, 1997. - 400 p.

12. Palmer D. Your dog. - M.: Mir. 1998 - 410 p.

13. Lukyanovsky V.A., Filippov Yu.M., Kopenkin E.P. and others. Diseases of dogs. - M.: Kolos, 1998. 310 p.

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Research data – Status praesens

General research

Temperature rect. 39ºСpulse 130 beats/minbreath 18 DD

Habit:

The position of the body in space is naturally standing.

The physique is correct, bone and muscle tissue are well developed, the body is proportional.

The fatness is satisfactory, the constitution is delicate.

Temperament is lively, good disposition.

Skin and subcutaneous tissue

The skin is clean, pink, elastic, moderately warm, turgor is preserved, skin moisture is moderate, corresponds to the norm, the smell is characteristic of an animal of this species. Sensitive to irritants, pathological changes, no rashes, skin integrity is not compromised.

The hairline corresponds to the norm, shiny, soft to the touch, well retained in the skin, thick, adjacent. Subcutaneous fat tissue is well and evenly developed.

Lymph nodes

Lymph nodes (inguinal, submandibular) are not enlarged, round in shape, smooth, mobile, elastic, dense, painless. There is no increase in local temperature, moderately warm.

Mucous membranes and conjunctiva

- the mucous membrane of the eyes is pale pink, the iris is yellow-green, evenly colored, the pupil is black, reacts to light. The mucous membrane is moist, without pathologies, there are no leaks, without violation of integrity.

- the mucous membrane of the nasal cavity is pale pink, without pigmentation, without pathological discharge, moist, temperature is normal, without damage to integrity.

- the mucous membrane of the oral cavity is pale pink with dark pigmentation, without ulcerations or pathologies, moist, without breaking its integrity. The smell of the oral cavity is normal.

Support-static apparatus

The placement of the limbs is correct, the joints are painless, symmetrical, movements are preserved in full, coordination is correct, without pathologies. There are no convulsions. The muscles are well developed, symmetrical, the muscles are toned, painless. There are no skeletal anomalies.

The bones are well developed, symmetrical, painless, without curvatures or fractures. The tail vertebrae are well developed, the tail is straight, without curvature. The ribs are in full volume, symmetrical, painless, smooth, the intercostal spaces are not enlarged.

Introduction

1. Brief information about demodicosis

1.1 Morphology of the pathogen and systematic position

1.2 Developmental biology

1.3 Pathogenesis

2. Diagnosis of demodicosis

2.1 Epizootiological and clinical data

2.2 Pathological changes

3. Organization of treatment and preventive measures

List of used literature

Introduction

Invasive diseases are widespread among animals, both domestic and wild.

1. Brief information about demodicosis

The causative agent of demodicosis was first described in 1845 by D. Gross.

Demodectic mites are morphologically similar to each other. In animals, mites develop in hair follicles and sebaceous glands, where they multiply and form colonies. Demodectic mites go through 4 phases in their development: egg, larva, nymphs (proto-, deutonymph), imago.

The entire development cycle of ticks from egg to adult takes 25-30 days. Outside the host's body, ticks live up to 9 days. Mobility is observed at 30-40° C.

Animals become infected through contact with sick people and through surrounding objects. All types of animals over 3 months of age are affected, but in dogs, cattle, sheep, goats, and pigs the disease occurs with complications.

Infection occurs through contact of healthy animals with sick ones and through surrounding objects. Young animals are most susceptible. The most dangerous period of spread is spring and summer.

For demodicosis, treatment should be comprehensive: specific therapy (use of acaricides) and systemic maintenance therapy, which necessarily includes the use of immunostimulants.

1.1 Morphology of the pathogen and systematic position

Phylum: Arthropoda

P/type: Chelicerata

Class: Arachnida

Order: Acariformes, Zoch.

Suborder: Trombidiformes, Reuter

N/family: Demodecoides, Bauns

Family: Demodicidae, Nik

The most common types:

Demodex canis are cigar-shaped mites with a cross-striated light gray cuticle. Body length: females 0.21-0.26 mm, males 0.2-0.22 mm. Body width: about 0.04mm. Juveniles are smaller in size, while mature females are the largest. Diamond-shaped eggs (0.068 - 0.083x0.019-0.033). The anterior pole of the egg is blunter, while the posterior pole is sharper and somewhat elongated. Larvae are 0.07-0.09 mm long, 0.025-0.03 mm wide. The body of the larva consists of two sections: gnathosoma and idiosome. Protonymphs are initially smaller than the larvae, and then their sizes increase (0.10-0.14x0.025-0.030); its body already consists of three sections. Deutonymphs are larger than other preimaginal stages (0.15-0.25x0.035-0.045). Their podosome is noticeably prominent, especially its ventral surface; on the ventral side, the coxosternal skeleton, the fourth pair of legs and the transverse striation of the body cuticle are clearly visible. Opisthosoma in the form of a short tail.

Demodex cornei - oval-shaped mites, much shorter than the first type, length 0.1 mm.

Demodex injai is a mite with a highly elongated body. Length: up to 0.6 mm.

1.2 Developmental biology

The development cycle is 25-30 days, with ticks going through 5 stages of development: egg, larva, protonymph, teleonymph, adult. The main invasive stage is females. Embryonic development inside the egg lasts 2-4 days. During metamorphosis, the preimaginal stages become inactive and stop feeding.

1.3 Pathogenesis

It has been established that the imago of D. canis, having penetrated from the surface of the skin into the hair canal of the follicle along the route, partially destroys the epithelial cells of the inner and outer root sheaths of the hair. In some places, the epithelium of the hair follicle disappears down to the basement membrane, between the connective tissue of the hair follicle and the epithelium of the outer root sheath. Having descended to the bottom of the hair follicle, the mite destroys the epithelial cells of the hair papilla, after which the inner hair sheath is no longer restored. By gradually cutting out the epithelium of the hair follicle, mites increase the volume of their container.

A similar picture is observed when D. canis mites colonize the sebaceous glands. The mite, passing along the inner wall of the lesion, and with the help of chelicerae, cuts off entire layers of cells, sometimes to the basement membrane and even deeper, leaving behind depressions in the form of grooves. The displacement of the basement membrane, and with it the connective membrane, deeper into the dermal tissue increases the volume of the lesion.

This picture is typical for the papular form of canine demodicosis. In this case, the mites rise up the canal, destroying the epithelium of the mouth in the neck of the former hair follicle along with the membrane, thereby interrupting the connection of the epithelium of the lesion with the epidermis. This leads to complete encapsulation of the mites and their death. Encapsulation also occurs in the sebaceous glands when mites destroy the epithelial wall of the lesion, as well as the underlying basement membrane and connective tissue membrane at the level of the entrance openings of the sebaceous glands.

2. Diagnostics

The diagnosis can only be made using special diagnostic methods.

To do this, several deep scrapings are performed, for which vegetable, glycerin or mineral oil is applied to the surface of the affected area. After 5 minutes of exposure, a scraping is made with the blunt surface of a scalpel until capillary blood, lymph and the contents of the follicles are released, tightly squeezing the skin fold.

The scraping is placed on a glass slide and microscoped using lactophenol, kerosene, and 5% alkali. Samples must be examined no later than 5 hours after they were taken. Permanent preparations are mounted in Berlise medium.

Indirect signs indicating deep destructive changes in the skin. When viewing preparations under a microscope, one should not only establish the presence of mites, but also determine which phases of development predominate, estimate the number of pathogens and draw a conclusion about the duration of the disease. These data are also important for developing a treatment strategy when choosing an acaricide and determining the frequency of its use. There may be an increase in the content of globulin fractions against the background of a decrease in albumin, an increase in glucose, urea, creatine and cholesterol in the blood of animals. The metabolism of copper, zinc and iron is disrupted against the background of an increase in the metalloproteins corresponding to these elements (transferin, ceruloplasmin, alkaline phosphatase, etc.). The degree of severity of biochemical indicators depends on the intensity of the invasion. These indicators can be used for prognosis, as well as as a control over the treatment methods used.

Making a differential diagnosis.

It is important to note that there are many diseases of various etiologies, the clinical signs of which are very similar to those of demodicosis. The most important among them are the following:

Cheyletiellosis is caused by thrombidiform mite of the genus Cheyletiella. Lesions on the skin in the form of dandruff along the entire length of the back.

Cold dermatitis usually occurs only in smooth-haired dogs. Dandruff, slight peeling of the skin, and brittle hair appear on the skin of the paws, face, and sides. Within a week the signs disappear.

True food allergy is an immunobiological disease of dogs of all breeds. Most often, skin pathology in this case comes down to itching and scratching, does not depend on the season, and is difficult to treat.

Clinical signs often manifest themselves in the form of a violation of the integrity of the skin, the appearance of bald areas on it in different parts of the body.

It has been proven that the disease is of an individual sensitivity nature, so a more precise diagnosis is made taking into account the results of a nutritional test, which uses diets with a limited number of components.

2.1 Epizootiological and clinical data

Demodicosis is a widespread disease of dogs observed in all countries with developed dog breeding. Demodicosis is recorded in dogs more often from 2 months of age to 3 years; the disease in older dogs is rare. Most often, the disease manifests itself in animals one year of age. The manifestation of the disease occurs with a decrease in temperature and insolation. In Russia, it is more often registered from autumn to spring. In southern countries, the disease is confined to the wet period of the year.

The disease is more common in short-haired dogs. Dogs with low and average body condition are most susceptible to the disease; dogs with above average body condition are less likely to become infected.

The disease is low contagious. Infection occurs only through contact; contamination of the environment does not matter. Currently, most authors are inclined to believe that contact transmission of the pathogen from a sick mother to a newborn is the main, if not the only, route of infection of animals. It was experimentally possible to infect healthy puppies with D. canis by placing them in groups with heavily infected puppies. (F. E. Frensch, 1976; F. Piotrowski et al., 1975). Dogs obtained by caesarean section and free from Demodectos became infected during prolonged application of the invasive material to moistened skin.

Apparently, the invasive stage is females, which, attacking a new host, penetrate the sebaceous glands and hair follicles of the skin and multiply intensively. A defect in the T-link of immunity leads to unlimited reproduction of ticks in immunocompromised animals and the manifestation of the disease. The remaining dogs become asymptomatic carriers.

It is believed that predisposing factors are heredity, stress, pregnancy, lactation, congenital and acquired immunodeficiency, long-term administration of corticosteroids. Apparently, high humidity, inadequate and insufficient feeding contribute to the manifestation of the disease.

Clinical signs. The development of the disease is usually chronic; with complications, symptoms accompanying the underlying disease can develop quite quickly. Based on the area of the lesion, localized and generalized forms of demodicosis are distinguished. Based on the localization of the process, pododemodecosis and otodemodecosis are distinguished. Based on the nature of the lesion, pustular (nodular), scaly (squamous) and mixed forms are distinguished. A separate nosoform is juvenile demodicosis - observed in dogs up to one year old.

Local demodicosis (scaly form). The most favorable course of the disease is if the disease affects puppies at about one year of age. The number of lesions does not exceed 4-5. There is no spread to the animal's body. There is no secondary microflora. This form occurs in up to 90% of cases of the disease. Most often, lesions occur around the eyes, forming characteristic “spectacles.” Erythema (local hyperemia) appears in the corners of the lips, on the muzzle from the forehead to the nostrils, on the neck, then on the chest and on the forelimbs, which is clearly noticeable in dogs with fair skin. Then expanding foci of coin-shaped depilation with a diameter of about 5 cm appear, less often diffuse, accompanied by fatty seborrhea with an unpleasant odor and parakeratosis (the appearance of scales). The hair follicles become clogged and hypertrophied as a result of intense sebum secretion, and blackheads (comedones) form. The skin becomes thickened and folded, often with bleeding cracks, its color has a reddish-blue or bluish-gray tint. There is no itching.

Generalized demodicosis. It is characterized by either a large number of foci of baldness (more than 5), or the spread of lesions to the entire body or at least the limbs, or, finally, the appearance of a microbial complication. This complication, as a rule, always occurs, which served as the basis for the name “pyodemodecosis” (demodex + pyodermatitis). This form is observed in 85% of cases in dogs older than 7 months and in 80% of cases in purebred individuals. The disease ends in self-recovery in less than 30% of cases.

Superficial dermatitis or bacterial folliculitis, which occurs with the disease, is characterized by the presence of numerous raised whitish pustules. They correspond to infected and hypertrophied hair follicles containing a white mixture of sebum and pus, replete with mites. The causative agents are most often Staphylococcus pyogenes albus (staphylodedecosis), but sometimes other bacteria (Pseudomonas aeroginosa, Proteus mirabilis).

Deep pyodermatitis, which is the next stage of microbial infection, is characterized by the spread of infection from the hair follicles to the dermis due to rupture of their walls. Depressed eggplant-colored boils with a diameter of 5 mm, filled with bloody pus, are observed. There are few mites in this pus. Demodicosis can also be purulent, accompanied by itching caused by the allergenic effect of microbial antigens.

The chronic form is expressed in skin alterations: hyperkeratosis (thickened, folded skin), seborrhea with a very strong odor. There is a significant deterioration in the general condition of the animal: adenomegaly (gland hypertrophy), emaciation, anorexia, apathy, renal failure due to the absorption of bacterial toxins. The animal may die with the phenomenon of cachexia and chroniosepsis. The course of demodicosis in dogs is usually chronic.

2.2 Pathological changes

A morphological examination of the skin of dogs reveals focal dystrophic, necrobiotic and necrotic processes, the nature of which depends on the intensity and form of the disease, and the inflammatory process is productive in nature. Tissue changes were detected in the emidermis, hair follicles, papillary and reticular layers of the dermis. The stratified squamous epithelium is ulcerated or flattened in limited areas. On the surface of these areas, purulent-necrotic or necrotic masses are determined. Many epithelial hair follicle orifices and hair follicles are dilated and contain mites and destroyed epithelial cells. In the multilayered squamous epithelium and the mouths of hair follicles there are foci of hyperkeratosis and parakeratosis. Around follicles with clusters of mites and a preserved wall of the outer root sheath, the cellular inflammatory reaction is very weak or absent.

When the wall of the hair follicle is destroyed and mites come into contact with the dermis, a cellular inflammatory reaction develops in it, and epithelioid granules are formed with the presence of giant multinucleated cells of the Pirogov-Langhans type and foreign bodies. The dermis contains massive inflammatory infiltrates and foci of varying sizes with a granulomatous structure. In areas of skin with necrosis in the epidermis, there is predominantly an inflammatory infiltrate, consisting mainly of granulocytes with a predominance of eosinophilic leukocytes, among which epithelioid 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 ticks, which consist of epithelioid and giant multinucleated cells with an admixture of lymphocytes, histiocytes, monocytes, plasma cells and eosinophilic leukocytes.

Demodectic mites are found in the cortical layer of the lymph nodes with generalized pyodedecosis. They are located in the marginal and cortical sinuses and peripheral areas of the lymphatic follicles. Granulomatous inflammation develops at the site of their penetration. Lymphatic follicles in the cortex are multiple, large, with wide light centers of reproduction and cell division patterns. In the lymph nodes there are signs of a cellular immune response with histiocytosis of the sinuses and hyperplasia of lymphoid follicles.

In the liver, in all cases, the same type of focal changes are noted, localized mainly in the portal tracts, periportal and perivascular. The portal tracts are significantly dilated as a result of edema, hemorrhage and a mild cellular infiltrate. In the peripheral parts of the lobules, the beam structure of the liver is disturbed, edema, hemorrhages, necrosis of groups of hepatocytes. Liver cells are in a state of diffuse protein dystrophy. Dead mites themselves can be found in the liver structures, penetrating from the skin into the lumen of large blood vessels. An acute inflammatory reaction of the liver is manifested by the development of hemocirculatory disorders and granulomatous hepatitis with the formation of tuberculoid-type granulomas. Sensitization processes and associated immune reactions most likely play a role in the development of granulomas.

In the kidneys, hemocirculatory disorders are found, expressed by uneven plethora of the cortical and medullary zones, noticeable dilation of blood vessels, edema and hemorrhages around some of them and focal fibrosis of the wall. The epithelium of convoluted tubules is in a state of granular and small-focal hydropic dystrophy. In the tubules of the medulla, small, few calcified cylinders are identified.

3. Organization of treatment and preventive measures

Treatment of any disease is carried out comprehensively. In the case of demodicosis, the veterinarian has two main methods at his disposal: pharmacotherapy and diet therapy.

Modern science offers many new insectoacaricides of different chemical groups. Multicomponent integrated tick control systems have been created; all that remains is to select the means and determine the regulations for their use. This is done individually for each animal.

Dogs other than collies, shelties and their crossbreeds are prescribed ivermectin preparations (ivomec, baymek, ivermage, ivermectin, novomec). The drug is given orally in a dose precisely calculated for the dog’s weight. The therapeutic dose for dogs is 0.6 mg per kg of live weight, based on the active substance. To determine the sensitivity of animals to the drug, the dose is increased gradually over several days. For puppies, the dose can be reduced to 0.4 mg/kg. The drug is given daily until the complete disappearance of mite eggs and larvae in the scrapings.

To monitor treatment, up to 5 scrapings are performed every 2-4 weeks. To control the dynamics, the number of mites in each sample is determined. Treatment is stopped only after two negative scrapings obtained with an interval of 3-4 weeks.

An alternative to ivermectin is milbemycin (“Interceptor”, milbemycin oxime) given orally to dogs older than 1 month at a dose of 1-2 mg/kg for 60-70 days.

Moxidectin (sidectin, cydectin) is administered orally at a dose of 0.4 mg per kg of live weight. The starting dose is increased from 0.1, which is increased to 0.4 mg per kg over 4 days. If signs of ataxia appear (up to 15% of animals), treatment is stopped. If the drug is well tolerated, the course is continued (from 42 to 120 days, on average 2.5 months).

Doramectin (“Dectomax”) is prescribed at a dose of 0.6 mg per kg of live weight weekly subcutaneously.

For dogs with hypersensitivity to macrocyclic lactones

Before starting treatment, hygienic treatment of the skin is carried out using 5% warm emulsion of soap K and zoo shampoo. The crusts are soaked with hydrogen peroxide. In the affected areas, the hair is shortened by carefully cutting it.

Amitraz suspension (Ectodex, Tactic) every two days for the first week, and then once a week for 1-2 months.

To use, 0.5 ml of the drug is diluted in a liter of water, applied with significant overlap of the affected areas of the coat. Improvement in clinical condition usually occurs three weeks after the start of treatment. Treatment continues for another 2 weeks, after receiving negative skin scraping test results. Recovery occurs in the absence of relapses 6 months after the start of treatment.

After acaricidal treatment, the dog can be fitted with an acaricidal collar that spreads amitraz (Preventuic). Amitraza can cause side effects, skin irritation, and even drowsiness. The latter disappears after a few hours (maximum 24 hours). In case of obvious intoxication, expressed not only in drowsiness, but also in bradycardia and hypothermia, a specific antidote atipamezole (“Antisedan”) can be used. Amitrase also has hyperglycemic effects, warranting caution in its use in diabetic animals.

Scheme of Larionov and Vasilevich. Subcutaneous administration of ivermectin in the form of a 1% solution at the rate of 0.3 ml/kg of animal weight. Purified sulfur, daily for 30 days with food at a dose of 40 mg/kg, for the scaly form - twice, for the generalized form - four times. External treatments with sulfur-tar liniment, consisting of: 2 parts of sulfur, 1 part of birch tar and 4 parts of tetravit. Treat daily for the first week, then once every 4 days for a month.

The effectiveness of treatment, depending on the form, appears 21-30 days after the start of treatment.

Contact insecticides, as well as various locally acting agents, are mostly ineffective - the penetration of the drugs into the hair follicles is limited. Thorough treatment of the entire coat with ointment-based preparations is labor-intensive and inconvenient for animal owners. Injections of macrocyclic lactones are not effective in monotherapy due to the inability to control a constant concentration in the animal’s blood.

Outdated remedies include iodine tincture, Vishnevsky ointment, and Yam ointment. Such treatments are repeated 2-4 times with an interval of 5-6 days. Use intravenously or subcutaneously of a 1% trypansini solution at a dose of 0.004-0.01 g per 1 kg of dog weight. The drug is injected 2 or 3 times, in severe cases 5 times with an interval of 3-6 days. At the same time, sedimentary sulfur powder is rubbed into the affected areas of the skin.

Prevention measures are limited:

1. Preventing dogs that have had demodicosis from being bred. Producers whose offspring include puppies affected by demodicosis should also be excluded from the list of producers;

2. Elimination of any temporary immunosuppression in puppies;

3. Use glucocorticoids to treat dogs under one year of age only for health reasons;

List of used literature

1. E. Benzior, D.N. Carlotti. Guide to demodicosis in dogs.//Veterinarian - 2000 - No. 3

2. A.D. Belov. Dog diseases. - 2nd edition, erased. - M.: Kolos, 1995

3. V.I. Romensky, A.A. Shinkarenko, Yu.F. Petrova, A.Yu. Gudkova Pathogenesis of demodicosis in dogs. // Veterinary Medicine - 2003.

4. Shustrova M.I. Demodectic mange in dogs. - St. Petersburg, 2001.

5. S.V. Larionov. Morphological features of Demodex mites and control measures for demodicosis.

7. S.V. Konyaev. Canine demodicosis.

Case history: Demodicosis in dogs. Case history of a dog successfully treated for demodicosis (difficult case)

Medications for illness

Folk remedies for demodicosis of the eyes

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Research data – Status praesens

General research