Increased body temperature in a cat. High temperature and fever in a cat

Keratinization (cornification, keratinization) is normal physiological process renewal of the epidermis, the outermost layer of skin, which occurs continuously throughout life. During the process of keratinization, epidermal cells from the lower basal layer, moving upward to the surface of the skin, are transformed into a nuclear-free dense stratum corneum - keratin (corneocytes). Horny keratin scales are constantly (and unnoticed by the eye) peeled off from the surface of the skin.

Keratin in the stratum corneum is the most important layer of the skin; it provides protection to the underlying layers of skin from mechanical damage, drying, ultraviolet radiation, penetration of microorganisms and allergens.

Among the disorders of keratinization processes, hyperkeratosis, hypokeratosis and dyskeratosis are distinguished.

Hyperkeratosis occurs most often and is characterized by thickening of the stratum corneum, i.e. accumulation of excess keratin on the surface of the skin. Clinically, this can be manifested by peeling, lichenification, and the appearance of horny growths. The rejection of scales of significant size and thickness is called exfoliation. Peeling is also called seborrhea (dry or oily), but this term is essentially misleading, because. speaks of increased sebum secretion, not excessive accumulation horny scales. Histologically or cytologically, but not visually, we can talk about the so-called. parakeratosis, when due to incomplete keratinization, nuclear corneocytes are present in the stratum corneum. When peeling, the scales are usually white or grayish in color. The presence of a yellowish or brown tint usually indicates the presence of a secondary bacterial or yeast infection.
Keratinization processes also occur in the hair follicle; follicular hyperkeratosis is clinically manifested by comedones and/or follicular casts.

Distinguish proliferative hyperkeratosis, associated with hyperplasia of the epidermis and accelerated progression of keratinocytes from the basal to the stratum corneum, and occurring much less frequently, retention hyperkeratosis due to strengthened bonds between keratinocytes (increased adhesiveness) and delayed rejection of horny scales from the skin surface.

Hypokeratosis It is much less common and may clinically manifest as excessively shiny skin (eg, paraneoplastic alopecia) or thinning of the skin.

Dyskeratosis characterized by premature pathological keratinization of individual keratinocytes, assessed histologically and occurs mainly in tumor processes in the epidermis (for example, in squamous cell carcinoma).

Disorders of keratinization processes are divided into congenital (eg, hereditary familial hyperkeratosis of the pads) and acquired (eg, acne), the latter being the most numerous.

Pathologies that I would like to dwell on in more detail are described below.

Ichthyosis

A group of hereditary primary pathologies of keratinization, the first signs of which (flaking, hyperkeratosis) become noticeable in early age. In practice, we most often encounter ichthyosis in golden retrievers, which have a mild, even sometimes transient, form of the disease, which, as a rule, does not in any way impair their quality of life.

The first clinical signs - excessive peeling of the skin, especially on the ventral parts of the body, become noticeable soon after birth. Ichthyosis can be encountered less frequently in other breeds; ichthyosis is most fully described and characterized in the American Bulldog, Great Dane, Jack Russell Terrier and Norfolk Terrier.

The final diagnosis will help to make histological examination affected skin and, in some cases (ichthyosis golden retrievers, Norfolk Terriers, American Bulldogs), DNA test.

Treatment is symptomatic - keratinolytic shampoos, moisturizers, and, if necessary, control of secondary infections.

Keratoconjunctivitis sicca and ichthyosiform dermatosis

This congenital pathology exclusively Cavalier King Charles Spaniels, inherited in an autosomal recessive manner and characterized by lesions of the skin and eyes.

Already at birth, affected puppies have a coarser and curly coat, and later symptoms of keratoconjunctivitis sicca (KCS), peeling skin, hyperkeratosis of the edges of the paw pads, deformed claws and onychomadesis become noticeable. Puppies experience pain when walking, and complications of SBS can occur in the form of secondary infections, corneal ulcers, and blindness. The diagnosis is not difficult to assume in the presence of congenital pathognomonic symptoms in this breed; histopathological examination and/or DNA testing is recommended for confirmation.

The prognosis is poor, because There is no effective treatment. IBS can be controlled with immunomodulatory/tear-stimulating treatment (cyclosporine eye drops).

Hyperkeratosis of the nose pads and nose

Characterized by excessive proliferation of the stratum corneum of the nose and/or paw pads. The affected surface is very thickened, dry, prone to cracking and secondary bacterial inflammation.

There are idiopathic (mainly in brachiocephalic breeds), senile (age-related) and hereditary hyperkeratosis.

Signs of hereditary, genetically determined hyperkeratosis usually become noticeable already at the age of 5-6 months. A distinction is made between nasal parakeratosis in Labradors and familial hyperkeratosis of the pads in Dogue de Bordeaux and Irish terriers.

Treatment is symptomatic - softening and removing horny growths, preventing cracking and infection.

Bengal nasal dermatitis

Hereditary pathology of Bengal cats, characterized by flaking and hyperkeratosis of the nose. The first signs of a “dry nose” are noticeable already at the age of several months. There is no itching or pain. Cracks and erosions may appear. Spontaneous remission is possible. Good effect showed 0.1% ointment with tacrolimus.

Spiculosis

This is a congenital pathology of the hair shaft of Kerry Blue Terriers, characterized by hyperkeratosis of individual hair follicles and the appearance at the age of 6-12 months of single hairs resembling thorns (Spicule: thorn, thorn). Their most common location is the heel area. The affected hair is thicker than the rest (up to 2.5 mm), hard and with an uneven surface, ranging from 0.5 to 3 cm in length. Spiculosis is observed mainly in males. And, although the presence of altered hair, as a rule, does not cause discomfort to the dog, pain and biting in this area, secondary bacterial infections are possible.

Follicular parakeratosis

This is a congenital progressive keratinization defect found in Rottweilers, Siberian Huskies, and Labradors and is characterized by generalized (muzzle, ears, torso) scaling and thick, wart-like crusts. Possible secondary infections and itching. In addition to skin lesions, puppies may also experience other congenital anomalies(myopathy, deafness, ophthalmological pathologies, etc.). An X-linked dominant mode of inheritance is suspected (only females are affected). The final diagnosis is based on histopathological examination of the skin. No effective treatment has been described. The prognosis is cautious and largely depends on the presence of pathologies of other organs.

Comedones in hairless dogs and cats

The skin of animals with congenital genetically determined hypotrichosis is predisposed to the formation of comedones and, as a consequence, to bacterial folliculitis/furunculosis.
Absence normal hair in the hair follicle and therefore difficult, untimely “evacuation” of keratinized follicular epithelium and secretion skin glands- a possible reason for this predisposition to blockage of the follicle mouth and the formation of a comedon.
Local medications with benzoyl peroxide and/or retinoids help to keep the situation under control. If necessary, GCS (glucocorticosteroids) are used to suppress the reaction to a foreign body (furunculosis) and antibacterial drugs.

Schnauzer comedone syndrome

This is a hereditary defect of follicular keratinization of miniature schnauzers, characterized by the appearance of multiple comedones in the occiput, dorsal neck and back in young or middle age. The course of comedo syndrome is often complicated by a secondary bacterial infection.
The diagnosis, taking into account the clinical picture and breed, is not difficult to make (be sure to exclude demodicosis!).

Treatment depends on the degree of manifestation of the syndrome: local keratinolytics (preparations with benzoyl peroxide, shampoos with sulfur and salicylic acid) +/- local (adapalene, tazarotene) or oral (isotretinoin 1.5-3 mg/kg) retinoids +/- antibacterial treatment.

Facial dermatitis of Persian cats

Otherwise known as “dirty face syndrome,” it is a rare disorder of keratinization processes in young Persian or Himalayan cats. Characterized by the appearance dark discharge on the muzzle, in the ear canal, around the anus. After the addition of a secondary bacterial +/- yeast infection, signs of inflammation (erythema, exudation, soreness) and itching appear.
Main differential diagnoses: allergy, dermatophytosis, demodicosis.

Most effective treatment Local or systemic use of calcineurin inhibitors (cyclosporine, tacrolimus) is recognized. At the same time, it is necessary to control the secondary infection.

Lethal acrodermatitis of bull terriers (LAD)

This is a rare congenital pathology, most likely associated with disorders of zinc and copper metabolism. It is characterized by growth retardation, an abnormally concave hard palate, progressive hyperkeratosis of the skin of the extremities and paronychia (acrodermatitis), chronic bacterial and yeast infections, diarrhea, pneumonia, and behavioral disturbances. Affected bull terriers have very low level IgA, which may cause recurrent infections. LAD is inherited in an autosomal recessive manner. Diagnosis is based on history, clinical signs and skin histopathology.

An effective treatment has not yet been found. Oral or parenteral treatment with zinc does not lead to improvement. To control secondary infections, local and/or systemic antimicrobials. GCS are generally effective in reducing skin inflammation.
With an average life expectancy of 7 months, death or euthanasia is usually caused by severe, intractable infections (bronchopneumonia and sepsis) and progressive debilitation.

There is no DNA test for diagnosis yet. Littermates and parents of affected puppies are not recommended for breeding.

Acne

Acne in cats- relatively common skin problem, characterized by the formation of comedones in the chin area and along the lip line. Comedones (acne) are a consequence of impaired follicular keratinization and excessive activity sebaceous glands- that is, it is a mixture of keratinized epithelium of hair follicles and sebum, which darkens when exposed to air and looks like “black dots” or “dirt” on the chin.

Acne can appear at any age; there is no breed or gender predisposition. The causes of acne are not completely clear. Acne may occur allergic dermatitis, dermatophytosis, demodicosis and more generalized keratinization disorders. Acne can appear due to stress. In some cases, acne is complicated by a bacterial infection and the clinical picture is complemented by papules, pustules and swelling of the chin.

Treatment involves finding and taking control primary cause, local use of benzoyl peroxide or retinoids, and, if necessary, local +/- systemic antibacterial treatment.

Acne in dogs, just like in cats, the phenomenon is not uncommon. Acne in dogs means folliculitis and furunculosis (papules, pustules, fistulas, often with hemorrhagic exudate) in the area of ​​the lips and chin. Young dogs of short-haired breeds (Doberman, Boxer, Bull Terrier, Mastiff, Great Dane) are predisposed. The primary cause may be follicular hyperkeratosis associated with local trauma, demodectic mange, or allergies.

Treatment consists of finding and taking control of the primary cause, local +/- systemic administration of AB and GCS.

Seborrhea of ​​the edges of the ears

This is a localized form of seborrhea that affects exclusively the edges ears from the lateral and medial sides. Lesions (alopecia, follicular casts) are bilateral. At chronic course These keratin growths can become so thick and hard that they crack, causing damage to the underlying skin, causing pain and often bleeding. The dog begins to shake its head and scratch its ears, which further aggravates the situation.
Dogs with floppy ears are predisposed, especially dachshunds, although the pathology can also be found in dogs with erect ears.
The reasons for the appearance of seborrhea are not completely clear; perhaps it is the result of ischemia.

Treatment is symptomatic - getting rid of crusts and regularly moisturizing these areas (creams with 10% urea). For inflammation - short-term use local drugs with an antibiotic and glucocorticosteroid.

Sebadenitis

This is a disease that is characterized by inflammation of the sebaceous glands of the skin and, as a result, deterioration in the quality of the coat, peeling of the skin and alopecia. It occurs primarily in dogs, although rare cases of sebadenitis have been reported in cats, rabbits and horses.
The sebaceous glands produce sebum, which excretory duct enters the mouth hair follicle, from where it is distributed over the stratum corneum of the skin and hair cuticle, forming a protective film that prevents moisture loss. In addition, sebum, due to the presence of fatty acids in its composition (linoleic, myristic, oleic and palmitic), also has antimicrobial properties.
Sebadenitis in dogs can be primary when sebaceous glands are the main and only target of the inflammatory process and secondary when they are involved in the inflammatory process “accidentally”, for example in such primary pathologies as leishmaniasis, demodicosis and uveo-dermatological syndrome.

This article will discuss primary sebadenitis, which is characterized by sterile T-lymphocytic inflammation of the sebaceous glands, which can result in their complete destruction.

The first signs of sebadenitis usually appear at the age of 2-4 years. Predisposed breeds include Akita Inu, Poodle, Samoyed, English Springer Spaniel, Hovawart, Vizsla and Havanese Bichon. There is no gender predisposition.
The causes and pathogenesis of sebadenitis are not fully understood. The lymphocytic nature of inflammation and a good response to immunomodulators give reason to assume an immune-mediated etiology, and the breed predisposition is heredity.

Clinical picture
Due to the lack of natural “lubricant,” wool becomes dull and brittle, and normal keratinization processes are disrupted, incl. follicular. Thus, characteristic features sebadenitis will cause hypotrichosis and alopecia, as well as peeling and the formation of voluminous follicular keratin casts, often “gluing” entire tufts of hair together. Skin lesions symmetrical and most pronounced in the forehead, back of the head, dorsal neck and back. The tail, due to severe alopecia, resembles a rat's. In breeds with long and curly hair (for example, poodles), the coat becomes shorter and loses its inherent curl. In short-haired dogs, such as the Vizsla, sebadenitis manifests itself a little differently, namely rounded, often merging areas of alopecia with peeling, involving the face, torso and even limbs.

The inner surface of the auricle itself ear canal are covered with dense scales, and earwax, due to the changed consistency and impaired self-cleaning mechanism of the outer ear, forms dry dark sulfur plugs predisposing to external otitis.

Sebadenitis is often complicated by secondary pyoderma, including deep pyoderma, which can significantly complicate the course of the disease, causing itching and pain.

The main differential diagnoses are demodicosis, dermatophytosis, bacterial folliculitis, zinc deficiency and endocrinopathies.
The diagnosis is based on the history, clinical picture and results of histopathological examination of the skin. For biopsy, areas with the most pronounced follicular casts, peeling and alopecia are selected. For acute process granulomatous or pyogranulomatous inflammation of the sebaceous glands is characteristic; chronic inflammation is characterized by the absence of sebaceous glands and perifollicular fibrosis.

Treatment and prognosis
With timely and proper treatment the prognosis is good. Patients with sebadenitis require lifelong therapy.
There are local and systemic therapy, both have approximately the same high efficiency in mono mode, but the best results can be achieved when using them simultaneously.

Local treatment is aimed at getting rid of flaking and follicular casts and restoring skin and coat affected by a lack of sebum. To do this, use keratolytic shampoos (for example, with benzoyl peroxide, salicylic acid and sulfur) followed by application to the skin baby oil for baths, diluted 50:50 with water. For the first 4-6 weeks of treatment, this procedure is carried out 1-2 times a week, then as needed, usually every 2-4 weeks. After achieving remission, you can try replacing the application of oil with spot-on fatty acids(Dermoscent Essential 6 spot-on, LDCA) or phytosphingosine (Douxo Seborrhea spot-on, Sogeval). To moisturize the skin between washes, you can use propylene glycol (diluted 50:50 with water).

Systemic treatment is aimed at reducing inflammation and restoring the sebaceous glands. Cyclosporine has been successfully used for this purpose. The initial dose is 5 mg/kg per day, after achieving significant remission (usually after 6-8 weeks) it is reduced to the minimum effective.

Supplementation with omega 3/omega 6 fatty acids or vitamin A (10,000-20,000 IU twice daily) and retinoids (eg, isotretinoin or acitritin 1 mg/kg 1-2 times daily) may also have a beneficial effect.
If a secondary bacterial or yeast infection is present, appropriate antimicrobial treatment is prescribed.
Glucocorticosteroids are not effective for sebadenitis.

Zinc deficiency

Zinc is an integral component of many metalloenzymes that regulate cellular metabolism. It is especially important for rapidly dividing cells such as epidermal cells. In addition, zinc takes part in the biosynthesis of fatty acids and the metabolism of vitamin A, and is necessary for normal operation immune system. Skin contains about 20% of total number zinc reserves in the body, and its highest concentrations are found in the keratinized layers of the nose and paw pads.

A lack of zinc in the body is largely manifested by dermatological symptoms. Latest Research There is a growing consensus that the pathogenesis of skin lesions is primarily associated with oxidative stress caused by free radicals, in the protection against which zinc plays an important role.

There are 2 zinc-dependent dermatosis (ZD) syndromes in dogs, both of which are relatively rare.
Syndrome 1 found mainly in Siberian Husky And Alaskan Malamutes, less common in other breeds (Samoyed, Bull Terrier, Pharaoh Hound) and is caused by a defect in the intestinal absorption of zinc. Accordingly, the appearance of disease symptoms is not directly related to a lack of zinc in the diet. The first manifestations of the disease become noticeable in at a young age(on average 1-3 years), and in severe cases and at the age of several weeks. Sometimes the defect in zinc absorption is so minor that symptoms of its deficiency will become noticeable only during stress, estrus, whelping or lactation.
Syndrome 2 observed in rapidly growing puppies mainly large breeds(Great Danes, Dobermans, german shepherds, Labradors, Rhodesian Ridgebacks, Bigdies, Boston Terriers and others). Lack of zinc in the body in the second syndrome is associated either with improper feeding(a diet low in zinc or a diet high in phytates or certain minerals (calcium, iron, copper) that interfere with the absorption of zinc), or with zinc loss due to disorders gastrointestinal tract. Zinc deficiency is also involved in pathogenesis genetic disease bull terriers - lethal acrodermatitis, which was discussed separately.

Clinical picture CDD is most often manifested by foci of erythema, alopecia, peeling, crusts and erosions in the muzzle (lips, dorsum of the nose, eyelids) and ears. The scabs may form a tight scab, with the skin underneath ulcerated. In severe or chronic cases, lesions can also occur in other locations - these are pressure points (elbows, heels), the borders of mucous membranes with the skin (vulva, prepuce, anus), paw pads. Skin lesions at the beginning of the disease can be unilateral, but then become bilateral and almost symmetrical. Characteristic lesions on the border with the nose are hyperkeratosis, erosions, crusts, hypopigmentation. Less commonly, the lobe itself and the claws with the claw fold are affected (onychomalacia, paronychia). Most dogs will experience mild to severe itching. Pyoderma and Malassezia dermatitis, as secondary infections, can significantly complicate the course of the disease.
Non-cutaneous manifestations are also possible - decreased appetite (partly due to an impaired sense of smell and taste), growth retardation and weight loss, lymphadenopathy, lethargy, conjunctivitis and keratitis.

Main differential diagnoses with minor manifestations (erythema, alopecia, peeling) there will be demodicosis and dermatophytosis, with itching - sarcoptic mange and allergies, and with severe cases - pemphigus foliaceus.

The diagnosis is based on the history, clinical picture and results of histopathological examination of the skin. The area of ​​the most pronounced peeling and hyperkeratosis is selected for biopsy. Erosive and ulcerated areas should be avoided, as the presence of the epidermis is important for diagnosis. The main change is pronounced diffuse follicular and epidermal parakeratosis.

Measuring serum zinc levels can only be used as an aid diagnostic method, since both false-negative and false-positive results are possible.

Treatment and prognosis. In case of syndrome 1, lifelong replacement therapy, but in most cases the prognosis is good, with the exception of severe cases that respond solely to intravenous administration zinc preparations. The initial dose of oral zinc is 2-3 mg/kg per day (preference should be given to methionine or zinc gluconate). It is better to crush the tablets to avoid vomiting and achieve maximum absorption. In most cases, significant improvement is observed within the first 4-6 weeks of treatment. If the initial dose is ineffective after 4 weeks of treatment, it is recommended to increase it by 50%.

You can also consider changing from one zinc preparation to another. In most cases, as maintenance therapy, after achieving stable remission, it will be possible to switch to significantly lower doses and even to taking zinc twice a week. In addition, to relieve inflammation, itching and improve the absorption of zinc at the beginning of treatment, glucocorticosteroids are indicated in an anti-inflammatory dose (an average of 0.5 mg/kg per day). Taking omega 3/omega 6 fatty acid supplements may also speed recovery. In heavy
or cases that do not respond to oral zinc, a slow intravenous administration of zinc sulfate diluted 1:1 with saline at a dose of 10-15 mg/kg is prescribed. One of the unwanted adverse reactions IV administration - cardiac arrhythmia. Injections are repeated at weekly intervals 4 times in a row, then the frequency of injections can be reduced by selecting the appropriate one for of this patient individual regimen to prevent relapses (once a month - 2 times a year).

An interesting observation is that sick bitches respond better to treatment after ovariohysterectomy. If necessary, appropriate antimicrobial treatment and keratolytic shampoos.

Sick animals should be excluded from breeding.

In syndrome 2, the prognosis is always good, animals quickly respond to the adjusted diet and, if they need additional zinc supplementation, it is not for long.

Svetlana Belova,
veterinary dermatologist (DipECVD)
Estonian University of Life Sciences

Cutaneous horn in cats is a rather rarely diagnosed pathology in traditional veterinary medicine, which is characterized by the appearance of a horn-like conical, cylindrical keratin growth up to 5 cm in length.

By appearance formation consisting of hard acellular keratin, reminiscent of a claw or horn of light or dark color. Most often in cats, the pads of the paws are affected, less often on the face, in the area of ​​the nose, eyelids, and genitals. The disease has a benign course.

Causes

As a rule, owners of furry purrs mistake the pathological growth for a second claw growing from the pad. Similar lesions in in rare cases cause concern, painful sensations, discomfort for pets. One or two paws may be affected. But do not forget that any deviations from the norm indicate malfunctions. internal organs.

According to veterinarians, similar pathology in cats, caused by excess keratin, may be due to individual characteristics animal body. Most often, the cutaneous horn in cats has viral etiology. Keratin benign growths on the paws occur due to the harmful effects of papillomaviruses.

Important! According to statistics, if treatment is not carried out, only 5 - 10% of pathological keratin formations become malignant.

Possible reasons:

• bacterial, viral infections, chronic diseases infectious etiology;
• malignant, benign neoplasms(basal cell carcinoma, sarcoma, squamous cell carcinoma, carcinoma);
• keratosis provoked by chemical and physical irritants (burns, injuries, claw infections);
• metabolic disorder in the body.

Cutaneous horn in veterinary practice most often diagnosed in the British, representatives Scottish breed. A keratin growth can appear in animals in the presence of the leukemia virus, as well as against the background of papillomas.

Diagnosis and treatment of cutaneous horn in cats

Diagnosis is made based on characteristic clinical symptoms, anamnesis data, serological, bacterioscopic studies carried out in the veterinary clinic. IN mandatory carry out screening for the presence of leukemia virus in the cat’s body and the necessary histological examinations. IN in doubtful cases a biopsy is performed differential diagnosis. All cats, without exception, must be examined for virus carriage.

Having noticed furry pet an uncharacteristic pathological keratin growth, you should not let the problem take its course, much less try to remove the skin horn. Any neoplasm provokes inflammatory processes in various structures of the dermis. Keratin growth destroys tissue and may grow uncontrollably. Adequate curative therapy can only be appointed after complex diagnostics, establishing the root cause.

Important! Despite the benign course, the prognosis depends on a number of reasons, the main root cause.

In most cases, treatment for cutaneous horn in cats involves surgery. Under the general local anesthesia surgical excision of the lesions is performed. In case of asymptomatic course, constant observation, medication is possible. symptomatic treatment. Cryo-laser therapy can be performed.

At mild form diseases, on initial stages veterinarians recommend treating cutaneous horn in cats with pharmacological agents (synthetic retinoids) that prevent further pathological growth. Four-legged patients may be prescribed:

• Azithromycin in tablet form.
• Acitrine. The drug is used under the strict supervision of a veterinarian.
• Aldara ointment. Apply a thin layer to the affected area three times a week. Rub the ointment until completely absorbed.

However, none of the above treatment methods provides a 100% guarantee that the growths will not appear again after some time. Pharmacological agents slow down, eliminate the processes of intense keratization, relieve inflammatory processes in the affected tissues.

Remember to do no harm for a pet, do not self-medicate. Effective therapy A veterinarian will select one for the fluffy.

Among the diseases of domestic animals there are all sorts: in some cases the pathologies are certainly fatal, while in others they only cause minor inconvenience. But there are other options... For example, hyperkeratosis in dogs. It doesn’t seem to pose an immediate danger to the dog’s life, but it also causes a lot of problems for the dog.

This is the name of the situation when skin on nose(nasal hyperkeratosis) or paws (digital hyperkeratosis) sharply thickens and becomes very rough. Mixed form– nasodigital hyperkeratosis. Let us immediately note that specific treatment this disease does not currently exist, but owners and a veterinarian can do everything to ensure that the animal’s quality of life remains at the same level.

This pathology occurs when the dog’s body begins to produce too much keratin. Digital hyperkeratosis is especially difficult, since the animal (in advanced cases) cannot even walk normally, not to mention running or playing outdoor games. If you look at a sick animal, it may seem that real “hooves” have grown on its nose or paws. The danger of this disease is not only that the affected nose or paws begin to perform their functions worse.

The fact is that normal canine anatomy and physiology simply “do not provide” for the presence of such thick and rough skin on these parts of the body. It dries a lot and then cracks. The wounds practically do not heal, becoming contaminated with pyogenic microflora. As a result - huge, non-healing ulcers and very high risk death from sepsis. If hyperkeratosis of the paw pads has reached this stage, the matter may end with their amputation.

Read also: Dysplasia in dogs - diagnosis and treatment

Why does this disease occur? What should it be differentiated from?

Unfortunately, hyperkeratosis is transmitted through genes. Labradors, black and Bedlington terriers are especially susceptible to this. For all these breeds, conscientious selection of sires is extremely important. If an animal exhibits hyperkeratosis, it should under no circumstances be allowed for breeding. Unfortunately, this is often neglected.

Hyperkeratosis is often noticed in the first year of a dog's life.. In any case, the first symptoms almost always appear before physiological maturity, approximately coinciding with the time of puberty. It is important to understand that the symptoms of hyperkeratosis can be very similar to the clinical manifestations of other diseases, some of which are very dangerous.

Fever is medical term, which refers to elevated temperature bodies. Normal body temperature for cats lies between 38.1° C and 39.2° C. The temperature is considered elevated if it rises above 39.7° C.

What are the causes of high fever?

Fever is initiated by the presence of pyrogens. Pyrogens can be endogenous (produced by the body) or exogenous (external). Pyrogens cause displacement normal temperature through the thermoregulation center located in the hypothalamus. After this, physiological reactions occur in the body that increase body temperature.

If this is a natural process, why does it cause problems?

Fever, or high temperature, can be good for the body because it inhibits the ability of viruses and bacteria to reproduce and improves the immune system's response to foreign bodies. However, if the body temperature remains high (over 40.5°C) for more than one or two days, the cat becomes weak and loses its appetite, which can lead to dehydration. If the temperature remains above 41.1° C, then cerebral edema and depression may develop. bone marrow, as well as blood clotting disorders.

A persistent high fever that persists for more than 48 hours is considered very serious and potentially life-threatening for a cat.

What are the clinical signs of fever?

Most cats with a high fever become lethargic and lose their appetite. Their heart rate and breathing increase.

How is fever diagnosed?

If your cat has a high fever, your veterinarian should check it thoroughly. medical checkup to check for any bites, lacerations, punctures and other injuries. In addition, extensive blood and urine tests may be required, as well as diagnostics of the thyroid gland.

What Causes Fever in Cats?

Most cases of fever in cats are caused by a viral infection such as feline immunodeficiency virus, feline leukemia virus or calicivirus. Many viral infections flare up and subside periodically, meaning that a seemingly healthy cat may experience a relapse within a week or two.

Bacterial infections can also cause fever, but they are usually accompanied by obvious injury or swelling. In addition, the infection can develop in chest cavity(pyothorax), in the kidneys (pyelonephritis), in abdominal cavity, oral cavity, due to tooth root abscess, etc. Much less commonly, fever occurs as a result of blunt trauma, lymphoma and other tumors, or due to fungal infections.

When diagnosing, it is important to tell the veterinarian the cat’s entire medical history, all recent trips, possible contacts with unknown or infected animals, food additives And medicines that you apply, as well as any other information that may be important.

How to treat high fever?

It is important to understand that diagnosing a high temperature (fever) will likely require extensive participation from you. The veterinarian must determine the specific cause of the fever in order to choose correct method treatment. In cases where a diagnosis has not been established, treatment will be initiated based on available information. Antibiotics are often prescribed to treat or prevent bacterial infection, which can develop as secondary. Drugs to reduce fever are rarely used. Nonsteroidal anti-inflammatory drugs for cats have been developed relatively recently. Acetylsalicylic acid (aspirin) and acetaminophen are very toxic to cats and should not be used without the approval of a veterinarian.

What is the prognosis for treating fever?

An accurate forecast can only be given when the exact cause of the high temperature is known. However, most cats respond well to supportive care, such as antibiotics and adequate water and food. Cats that present with periodic fevers should be properly evaluated and treated before permanent damage occurs.