Prevention of infectious diseases of fur-bearing animals. Abstract of hematuria and wetting of minks. sable anthrax

1. Mink hematuria

MINK HEMATURIA (Haematuria lutreolarum) is a disease characterized by the appearance of blood in the urine and anemia. Mostly puppies get sick after jigging.
Etiology.
The causes of blood in the urine are: acute food intoxication, deficiency of vitamins A, E, hereditary muscular dystrophy, inflammation of the urinary tract and urolithiasis, glomerulonephritis, external stimuli (sharp violent catching, mating), tumors in the genitourinary system, and in newborn fox puppies and arctic foxes - hemorrhagic diathesis (red foot, hypovitaminosis C).

Pathogenesis.
Toxic substances, released through the urinary system, act on the receptor apparatus of the mucous membrane of the bladder, cause the expansion of the capillaries of the mucous layer, followed by the release of blood. Prolonged blood loss leads to the development of severe chronic posthemorrhagic anemia with all the ensuing consequences.
Against the background of anemia, degenerative changes develop in the liver, kidneys and other organs.
As a result of constant blood loss, depletion of calcium, phosphorus, chlorine, iron, copper and protein in the body occurs, which leads to a violation of bone marrow hematopoiesis,

Symptoms.
Urine is brightly bloody and contains blood. In many cases, it turns brown. Depending on the etiology, other signs may also develop - loss of appetite, depression, diarrhea, abortion, anemic visible areas of the mucous membranes and skin, frequent and painful urination, an increase in the volume of the bladder (set by palpation) and bloody-purulent discharge. In newborn puppies, swelling and cyanosis of the crumbs of the paws are noted.

Pathological changes
Characterized by pinpoint hemorrhages under the capsule and in the renal parenchyma. The kidneys are not enlarged, the consistency is flabby, they are colored paler than usual. The bladder is distended, filled with red-yellow urine, which contains a yellow sediment.

Forecast.
Adverse. With abundant blood loss and exhaustion, the death of animals occurs.
Diagnosis.
Symptoms of the disease are characteristic, but it is necessary to establish the main cause of its occurrence. So, with a deficiency of vitamin E, a significant number of animals suffer. Urine is usually brown. At autopsy of dead animals, skeletal and cardiac muscles are pale, dystrophic, subcutaneous fat is yellow or anemic. The seasonality of the disease is weakly expressed. A high percentage of missing females, analysis of diets and feeds indicate an overload of diets with fat or the use of oxidized fat with insufficient supply of vitamin E. In case of feed intoxication, along with bloody urine, most animals show other symptoms - loss of appetite and diarrhea, and the number of patients with these signs does not increase gradually, but quickly.
With urocystitis and urolithiasis, strict seasonality is characteristic (mainly July-August), mainly male mink puppies are affected, and the disease, despite some coverage of livestock, still remains sporadic and subsides by autumn. Some irritants (forcible capture of an animal, mating) cause hemorrhages in the organs of the urinary system. In case of delayed emptying of the bladder, the urine becomes brown. This disease usually occurs only during the rut in the form of individual cases. Male foxes and arctic foxes are more commonly affected.
In the case of tumors, the incidence is single. Red-footedness is observed in puppies under the age of 5 days. Hereditary muscular dystrophy is differentiated using pathohistological studies for the presence of different diameters of myofibrils in a transverse section of skeletal muscles, degenerative processes and phagocytosis of myofibrils, basophilia of their sarcoplasm, etc.

Treatment and prevention.
Treatment is ineffective. Eliminate the main cause of the disease, most often vitamin E deficiency and feed poisoning. Blood transfusion, calcium chloride can be used to stop bleeding. Assign a diet of feed rich in vitamins A, B 1, B 12, C. Therapeutic measures provide only a temporary improvement. They feed foods rich in vitamin E (meat, milk, liver, various fats and oils).

2. Wetting minks
Wetting minks (dysuria). A pathological condition that is characterized by a violation of the physical properties of urine, as a result of which it spreads over the animal's stomach, affecting the skin and hairline. Males of fur-bearing animals of various species are ill mainly, more often minks, sables and foxes. Abroad, the disease is known as "wet belly" (wet belly). The disease causes damage to the skins and death of animals.
History reference. For the first time in Russia, “wetting” of minks was described by S. Ya. Lyubashenko in 1984. Based on the study of epizootology, the clinical and pathoanatomical picture of the disease, as well as experimental data, he came to the conclusion that “wetting” is an independent disease of bacterial etiology. In 1953, Lyubashenko managed to isolate pyogenic microflora from the bladder and kidneys of minks that had fallen with signs of “wetting”. The isolated streptococci, staphylococci and Pseudomonas aeruginosa had high properties when infecting minks and laboratory animals.
In 1962-1964, S.K. Gunn, who studied the causes of impaired urination in minks, also confirmed the bacterial etiology of the disease and came to the conclusion that “wetting” is due to Proteus mirailis bacteria, which are found in the prepuce of sick males.
According to Schaible P. J. Aulerlich (1963), the disease develops in females only during pregnancy and lactation, and in young males during the period of intensive growth and development of the hairline. W. Z. Leoschke (1952-1959), who studied the relationship between impaired urination and feeding of animals, found that the number of cases of "wetting" in minks occurs when animals are excessively fed fat.
S. Ya. Lyubashenko (1949-1950), on the basis of surveys, proved that the largest percentage (up to 32) of sick minks is among young animals in June, July and August. A case of disease in puppies under the age of 10-15 days has been noted.
According to C. K. Gunn (1962), up to 20-40% of males are sick in disadvantaged animal farms, and up to 0.9% of females.
Studies by G. M. Diveeva and G. A. Kuznetsov (1965-1968) showed that “wetting” among minks in some farms reaches 4.5%, and in others 13.9%, and this disease is observed more often among colored minks .
Recently, scientists from foreign countries and Russia have paid attention to the high susceptibility to the disease of minks of certain lines and color groups, which indicates the likelihood of a hereditary predisposition to "wetting".

Etiology and pathogenesis.
The causes of the disease have not been fully elucidated. The disease is possible with a lack of carbohydrate feed in the diet of the animal and a simultaneous excess of fat. When fats are broken down, dicarbosyl acids are formed, which, excreted in the urine, contribute to its easy absorption into the hairline. Of certain importance is the ratio of calcium, phosphorus and fat in feed. With an excess of calcium and fat, sparingly soluble soaps are formed. Excreted with urine, they reduce its surface tension, and urine during urination spreads over the skin. In constantly wetted areas, the skin becomes inflamed, the hair turns yellow-orange, falls out, which greatly devalues ​​the fur.
It has been noted that dysuria occurs when animals are fed with bacteria-infected (Proteus, mirdilis, coli, etc.) offal, heads and entrails of birds, as well as poor-quality fish; it is quite often observed with a lack of vitamins H (biotin) and A. Wetting is also observed with urolithiasis and cystitis and may be the result of stress.
Symptoms.
In sick minks, frequent involuntary urination is observed. The hairline in the area of ​​the perineum, abdomen and the inner part of the hind limbs in the initial period of the disease is strongly moistened, and later the hair in these places sticks together. Gradually, the skin turns red and swells sharply, soon small pustules appear on it, which open up, and ulcers form in their places. With the further development of the process on the affected areas of the skin, the hair falls out, the skin becomes compacted, coarsened, and then necrotic lesions appear, mainly on the abdomen and in the prepuce. Skin necrosis spreads, quickly captures the skin of the inner surface of the hind limbs and abdomen. Often, inflammation of the prepuce develops in the future. This is manifested by its strong swelling, and the outlet closes. The excreted urine is retained in the preputial sac, the act of urination is disturbed, the animal experiences severe pain.
In some cases, "wetting" can be manifested only by limited moistening of the hairline in the perineum and abdomen. This symptom is observed for only a few days (2-5), and then urination is restored, the hairline gradually dries up, and the process ends with the complete recovery of the animal. In such cases, mink urine is usually clear.
In the presence of purulent cystitis, which is observed quite often in severe cases of the disease, containing a significant amount of blood cells, epithelium of the bladder mucosa, sometimes necrotic pieces of the bladder mucosa and a large number of different microflora (cocci, rods).
In contrast to urolithiasis, urine when "wetting" the acid reaction.
Sometimes, with purulent cystitis, the inflammatory process can go to the abdominal, cause purulent peritonitis and the rapid death of the animal.
pathological changes.
Corpses are often of satisfactory fatness and less often emaciated. The hairline in the crotch area, the abdomen is wet, glued into dense bundles, in some places the hair fell out. On bald areas, the skin is thickened, dense to the touch, sometimes necrotic. With necrosis, ulcerative lesions of certain areas of the skin are noted, especially in the perineum and abdomen, less often the chest.
Changes in the organs are very diverse, but most often they manifest themselves in the lungs with varying degrees of hemorrhage, sometimes in the form of pneumatic foci, in the liver - degenerative changes, as a result of which it acquires a clay color and a flabby consistency. The spleen is slightly swollen, with occasional necrotic foci. Lymph nodes and especially swollen mesenteric ones are enlarged in size, sometimes petechial hemorrhages are noted on their surface. The kidneys are enlarged, sometimes the renal capsule is thickened, often fused with the cortical layer. The surface of the kidneys is variegated, while yellowish-gray islands are visible against a brown-red background, occasionally spotted hemorrhages are found. The renal pelvis is dilated, contains a dirty gray or bloody fluid mixed with pus. The ureters are thickened. Quite often, purulent cystitis is established. In the mucous membrane of the bladder, banded or spotted hemorrhages are observed. Bladder stones are rare.
Diagnosis.
The presence of animals suffering from impaired urination is a sufficient basis for making a diagnosis. To clarify it resort to laboratory research. For this purpose, bacteriological cultures are made for MPB, MPA and MPPB from freshly excreted urine, pustules and necrotic ulcers, and from fallen minks from the bladder, kidneys, liver, heart and spleen.
In crops from urine, in most cases, a mixed culture is isolated, mainly gram-positive cocci, diplococci, Escherichia coli, Pseudomonas aeruginosa. It should be borne in mind that a variety of microflora is released at different periods of the disease: at first, Escherichia coli or Pseudomonas aeruginosa may prevail, later coccal forms, or vice versa.
Treatment.
They present good conditions to the sick animal. Poor-quality, seeded with pathogenic microflora feed is excluded from the diet, they give easily digestible and rich in vitamin composition feed: milk, cottage cheese, skim milk and fresh muscle meat. When the bladder is inflamed, water is given in abundance.
Urotropin and antibiotics are used with food for 10-15 days.
Prevention.
Complete feeding with benign feed, rich in vitamins, proteins and other substances, which helps to increase the resistance of the organism as a whole and the urinary system in particular.

Bibliography
1. Bazhenov S. V. Veterinary toxicology. - M: State publishing house of agricultural literature, 1958.
2. Berestov V.A. Tutorial. - St. Petersburg: Lan, 2002. - 480 p., ill., 1 incl. - (Textbook for universities. Special literature).
3. Danilov E. P. Diseases of fur animals / E. P. Danilov, A. I. Mayorov, V. A. Chizhov and others; Ed. E. P. Danilova. - 3rd ed., revised. and additional - M.: Kolos, 1984. - 336 p., ill.
4. Kondrakhin I. P., Levchenko V. I., Talanov G. A. Handbook of a veterinary therapist and toxicologist: Handbook / Ed. prof. I. P. Kondrakhin. - M.: KolosS, 2005. - 544 p.
5. Kopeikin I. G. Diseases of fur animals. - Chita, 2002.
6. Lyubashenko S. Ya. Diseases of fur animals. Ed. 2nd, revised. and additional Ed. With Y. Lyubashenko. M.: KolosS, 1973.
7. Khmelnitsky G. A. Veterinary toxicology / G. A. Khmelnitsky, V. N. Loktinov, D. D. Poloz. - M .: Agropromizdat, 1987. - 319 p., L. ill.: ill. - (Textbooks and teaching aids for students of higher educational institutions).
8. Shcherbakov G.G., Korobov A.V. Internal diseases of animals. - St. Petersburg: Publishing house "Lan", 2002. - 736 p. - (Textbooks for universities. Special literature).

V.I.Ulasov
vgnki

The state of veterinary well-being of the country's caged fur farming is an "iceberg" phenomenon, the visible part of which are cases of manifestations of certain diseases, while its underwater part remains without due attention.

The visible part of the problem is massive diarrhea and Aleutian mink disease. Of course, viral enteritis (VEN) is easily confused with gastroenteritis of alimentary origin, although the etiology of these diseases is different. VEI most often begins with a focal disease of minks and never stops after replacing feeds with benign ones. According to our data and foreign data, the VEN pathogen has over 98.5% genome homology with other parvoviruses of carnivores, but high antigenic variability is expressed.

According to American researchers, the rate of genetic variability in WEN is 2 * 10" nucleotides per year, and even differences in 11 nucleotides lead to a change in the host of this virus.

Testing of blood sera from unvaccinated minks shows that the number of seropositive animals in the farms is increasing every year. This circumstance is confirmed by the results of a study of excrement for the presence of a hemagglutinating agent, which is identified in RTGA as parvovirus. We believe that cats living in fur farms and, apparently, dogs, which are latent carriers of this virus, contribute to this in many respects.

The data available to us convince us that hyperimmunization of mink females, in whose intestines the virus resides for a long time and is periodically released into the external environment with feces, also contributes to the high carriage of the virus, especially under stress.

Of no small importance in maintaining epizootological well-being according to VEN is the importation of animals from breeding farms, which no one examines for virus carriers.

In addition, the causative agent of the disease is able to persist for a long time at the objects of veterinary supervision. The conditions of keeping, the lack of reliable heat treatment of feed, irregular disinfection and decontamination of animal care items are predisposing factors in the spread of infectious diseases of minks.

The resistance of vaccinated mink puppies to infection with epizootic VEN strains also depends on the presence of colostral antibodies at the time of immunization. There is indisputable evidence that colostral antibodies in puppies obtained from old females persist up to 3 months of age, while in young animals obtained from mothers of the first year of whelping, they persist for no more than 5 weeks. Moreover, these indicators are negatively affected by the defeat of animals with the Aleutian mink disease (ABN) and the use of feed contaminated with mycotoxins. Experimental studies have shown that when the titer of colostral antibodies in RTGA is not higher than 1:8, a third of the vaccinated minks fell ill after infection with VEN strains.

The most acceptable to start vaccination is 3 - 4 months of age, but given the complexity of the situation in animal farms for this disease and, especially, for botulism, vaccination of puppies in the Russian Federation and abroad begins at 55 - 60 days of age. In order to get out of the situation with viral enteritis, the content of this antigen in the grafting dose of a commercial vaccine has been significantly increased in recent years.

It is well known that the diagnosis of any disease should be comprehensive and based on epizootological data, clinical signs, pathological changes with mandatory confirmation by laboratory tests.

The most recognized worldwide is the indication of the virus in the mucous membrane or feces of diseased minks in RGA or using electron microscopy. At the same time, the appearance of non-hemagglutinating isolates of the pathogen is not excluded, as there are limited publications abroad. For the final confirmation of the identity of the isolated isolate, RTGA is required. Despite their advantages, RGA and RTGA have disadvantages due to the presence of porcine or green monkey erythrocytes (abroad), as well as the study of material samples at the late stages of the disease, when coproantibodies are formed.

Isolation of the virus in various cell cultures has not found its practical application, since virus isolates do not have cytopathogenic activity, and RHA must be used to detect the virus.

An appropriate ELISA kit for diagnosing parvovirus infections in carnivores turned out to be in demand at the very beginning of the disease. In the later stages, when the concentration of the virus decreases due to neutralization by local antibodies, a positive reaction in the ELISA may fall out.

In recent years, the interest of researchers in the use of PCR for the diagnosis of many, including chronic and persistent, diseases of fur animals has increased significantly. Apparently, in addition to stating this fact, it is extremely important to differentiate the vaccine strain from the field isolate, to exclude the possibility of false positive reactions due to sampling of the material on the farm and during research.

The subject of discussion is the method of indication of specific antibodies in RTGA in the blood sera of spontaneously sick or vaccinated animals. The available data give grounds to unambiguously assert that the study of antibodies does not give grounds to speak about the diagnosis of VEN. With regard to the study of the intensity of post-vaccination immunity, it should be noted that these antibody studies can be reliable only in the case of the study of paired sera taken from the same animals with an interval of 2-3 weeks.

Thanks to previous work, the epizootic situation for mink pseudomonosis has significantly improved. At the same time, we have isolates of this microbe that are not typed with a set of 12 serotype sera from the Khabs collection. To eliminate this circumstance, an additional set was developed, consisting of 20 serotype diagnostic sera. With regard to the isolation of Pseudomonas aeruginosa from sick foxes and arctic foxes, we can say that, in our opinion, it plays a secondary role in the appearance of pathology in these species of fur-bearing animals.

P. aeruginosa transmission factors are infected soil and water, in which this saprophyte persists, accumulates, possibly changing the serotype and degree of sensitivity to a number of antibiotics and disinfectants. The microbe is often found in human and animal feces, on body surfaces, on the external genitalia, as well as in feed, bedding and water, with the same serotypes that cause the disease. At the same time, the question of what is necessary for the activation of P. aeruginosa in the body of warm-blooded animals remains unresolved. We believe that the above factors largely contribute to this, as evidenced, as a rule, by unsuccessful experimental attempts to reproduce the disease in piglets, foxes, and arctic foxes.

The uncontrolled use of antibiotics that suppress the development of competitive symbiotic microorganisms contributes to the fact that Pseudomonas aeruginosa, as a saprophyte that is insensitive to most antibacterial drugs, begins to multiply rapidly, causing a pathological process in the body. Very often, Pseudomonas aeruginosa is isolated in association with enterobacteria and other conditionally pathogenic flora.

Regardless of the object or animal species from which the isolate of the pathogen was isolated, all pseudomonads are presented in the form of straight gram-negative rods with rounded ends. They weakly ferment glucose, do not decompose mannitol and fibrin, do not coagulate milk, but dilute gelatin, about 15% do not form or form the pigment pyocyanin in a small amount.

The virulence of different isolates and strains of P. aeruginosa varied depending on the method of infection and the type of experimental animals. Most isolates of the pathogen were not very sensitive in the disk diffusion test with penicillin, but there was a zone of inhibition of their growth around the disks with gentamycin.

Of all domestic and farm animals, the use of active specific prophylaxis is expedient and justified only in caged minks. The strains of serotypes 05, 06, 08 and 011 selected in the antigen-optimal ratio in the commercial vaccine "Bionor" make it possible to prevent the occurrence of Pseudomonas aeruginosa infection for a long period.

Based on the foregoing, in the system of measures to combat Pseudomonas aeruginosa infection in the country, it is justified to conduct active prophylactic immunization only in minks using associated vaccines containing the required number of pathogen serotypes encountered. However, due to the wide serotype variability, constant monitoring of strains circulating in nature is required to determine their serovariable composition.

Aleutian mink disease (AMD) is also caused by a carnivore parvovirus that is genetically and antigenically distinct from other carnivore parvoviruses of the feline and canine families. We believe that field isolates of the ABN virus are antigenically equivalent, but differ in virulence.

In the domestic specialized literature, mainly classical forms of the course are described, which is manifested by a noticeable decrease in the birth rate, a significant increase in the sensitivity of affected animals to other pathogens, and an increase in mink mortality on infected farms.

Available observations show that chronic forms of AD are recorded locally, especially in puppies obtained from seronegative females. Newborn puppies die from acute interstitial pneumonia, parenchymal hemorrhage and severe atelectasis.

Worldwide, the most effective methods of combating this disease are the identification, isolation and subsequent slaughter of positively responding animals. The tissue antigen for RIOEF proposed by V.S. Slugin in 1975 is the most specific and active in comparison with the previously used histopathological studies and the iodine test. During the application of this method, a number of farms have been improved, while its effectiveness in newly emerging epizootic foci and stationary disadvantaged farms is different. At certain stages of the development of the infectious process in minks, RIOEF completely disappears.

Comparison of the data on the annual amount of antigen produced and the presence of animals in the country's farms gives grounds to assert that local veterinarians ignore the implementation of the Instructions for combating Aleutian mink disease in terms of covering the entire livestock with diagnostic studies.

In our opinion, the diagnosticum produced for RIOEF also needs to be improved. Its activity should be increased, since at a high antibody titer in spontaneously diseased minks, an antigen with an activity of 1:4 does not form a precipitation line in RIOEF. In Denmark, a similar antigen is released with an activity of 1:16. It is long overdue that in the production of this antigen to switch from tissue antigen to a more advanced cultural one, which excludes infection of minks in farms.

The underwater part of the "iceberg" is represented by problems that arose after the liquidation of the unified leading centers of fur farming (Zveroprom, Tsentrkooppushnina, etc.), but the newly emerged associations are busy solving completely different issues.

On the ground, the availability of information has noticeably decreased, even scientific and production publications, such as the journals "Veterinary Medicine", "Rabbit Breeding and Fur Breeding", are not available on all farms, and the publication of the International Association of Fur Breeders, the journal "Sentifur", has become a bibliographic rarity even for scientific and research institutions. It is necessary to expand the work of advanced training courses for veterinary specialists, to revive the holding of seminars, scientific and production conferences with the involvement of managers and animal specialists of farms, to develop and approve Veterinary and sanitary requirements for fur farms.

Fur farms no longer receive copies of instructions, instructions, information letters and orders. Guiding documents on veterinary medicine have ceased to be published, many instructions for combating certain diseases of fur animals and rabbits are obsolete and do not contribute to their elimination (toxoplasmosis, tuberculosis, infectious encephalopathy, ringworm, scabies, etc.).

Due to the lack of funding and specialization of scientific institutions and the regional veterinary service on the pathology of fur-bearing animals and rabbits, monitoring of common diseases is not properly carried out. Often, fur farms classified as breeding farms turn out to be unfavorable for ABN and other infectious diseases.

Long-term experience of domestic fur farming has shown that the high productivity of fur-bearing animals can be achieved only after they are provided with high-quality feed and drinking water. Meanwhile, indicators of the good quality of feed have not yet been approved and are interpreted differently on the ground. Moreover, the domestic values ​​of these tests are not comparable with foreign ones, which is especially evident when importing feed.

An experimental verification of the change in the timing of the start of mink vaccination is required, taking into account recent achievements and practical observations, as well as the creation of an anti-epizootic stock of medicines for emergency use if necessary.

The prevention of common diseases of fur-bearing animals can be achieved by rigorous implementation of reasoned specific and general veterinary and sanitary measures.

magazine "Veterinary" №05 2008

During lactation, animals should be provided with plenty of drinking water. With insufficient water intake in females, milk production stops and the body can become dehydrated, which contributes to the development of lactation exhaustion. Table salt is started to be given after whelping is completed on the farm and is stopped 2 weeks after the young stock is deposited.

DISEASES OF THE URINARY SYSTEM

Dysuria(wetting) - a common disease, accompanied by a disorder of urination due to a deep metabolic disorder. Found in fur animals

All kinds and causes great damage to farms as a result of deterioration in the quality of skins and the death of animals. Abroad known as "wet belly" (wet belly).

In sable puppies of post-weaning age with identical signs, diaper rash occurs, unjustifiably called wetting. Diaper rash occurs from the third decade of May in cases where measures are not taken to improve the ventilation of the houses (the wooden covers and bottoms are not removed). The course of the disease is often benign. However, sables, like other animals, can also suffer from typical dysuria.

Etiology and pathogenesis. Primary dysuria occurs when there is an excess of fat and calcium in the feed and a lack of carbohydrates. As a result, metabolism is disturbed and sparingly soluble soaps are formed, which reduce the surface tension of urine. Therefore, urine is not excreted in a trickle, but in drops, spreading over the stomach, absorbed by the hair and irritating the skin. Of great importance in the etiology of the disease is, along with the overload of the diet with fat, the use of feed with oxidized fat. However, in both cases, similar mechanisms for the development of the disease are included - a deficiency of many vitamins (due to large expenditures or oxidation), which makes it possible to consider dysuria as one of the manifestations of hepatosis, polyhypovitaminosis and feed intoxication.

Secondary dysuria occurs when animals are fed conditionally suitable and poor-quality feed (infected with Proteus, Escherichia, etc.), with urocystitis and urolithiasis, urethral cysts, stress, biotin deficiency, salmonellosis, paresis of the back belt and other diseases.

Symptoms. In sick animals, urine is excreted almost continuously. From constant hydration, the skin in the abdomen, perineum and inner surface of the pelvic limbs becomes macerated and inflamed, the hair becomes wet, acquires a yellow-brown color. Animals emit a strong odor. They lose weight and lose their appetite. Late in the disease, induration and ulceration of the skin, often inflammation of the prepuce, paresis of the pelvic limbs, emaciation, and death are noted. With secondary dysuria, signs of the main

With sable diaper rash, wet hair is found in the abdomen and the inner surface of the pelvic limbs. Later, in these areas, the skin becomes red, slightly edematous. The epidermis is torn off, and small weeping foci are found, which are sometimes covered with purulent exudate. Animals are thinner. When moving, they sort out the pelvic limbs and stoop. Very often, sick puppies run only on their front legs, and imitate movement with their raised hind legs. In some years, a large number of puppies get sick. The illness usually lasts 2 weeks.

Diagnosis. Set according to characteristics

Treatment. Sick animals are injected with a mixture of vitamins

group B, glucose, aminopeptide, hexamethylene-tetramine, sulfamonometoxin and other antimicrobial agents, 5-10 drops of Eleutherococcus tincture are given orally. Locally, the wound or skin is treated with a 3% hydrogen peroxide solution, septonex, penicillin solution and powdered with a fine powder (chlortetracycline).

Prevention. Do not allow excess fat in the diet. Feed only benign fats. In the autumn and winter-spring periods, the fat content should not exceed 4.5 g, and in the summer - 5.5 g per 100 kcal of feed. A sufficient amount of carbohydrate feed is introduced into the diet - boiled potatoes, cabbage, carrots, etc. Otherwise, the prevention of primary dysuria is the same as with hepatosis, polyhypovitaminosis and intoxication. It is necessary that the rations contain a sufficient amount of vitamin E and that the animals are given plenty of water. To prevent sable diaper rash, the wooden covers of the houses should be kept open from about mid-May. With the onset of warm nights, it is necessary to remove the wooden bottoms from the houses, leaving only the mesh ones.

Hematuria is a symptom complex of various diseases characterized by the admixture of blood in the urine. In fur farms it is registered everywhere, especially often get sick

foxes, foxes, minks.

Etiology. The reasons for the appearance of blood in the urine include: acute feed intoxication, vitamin E deficiency, hereditary muscular dystrophy, inflammation of the urinary tract and urolithiasis (urocystitis, pyelonephritis, urolithiasis), external stimuli (sharp violent catching, mating), tumors in the genitourinary system , and in newborn puppies of foxes and arctic foxes - hemorrhagic diathesis (red paws, hypovitaminosis C).

Symptoms. In animals, urine is colored bright bloody or contains an admixture of blood. In many cases, it turns brown. Depending on the etiology, other signs may develop - loss of appetite, depression, diarrhea, abortion, anemic visible areas of the mucous membranes and skin, frequent and painful urination, an increase in the volume of the bladder (set by palpation) and bloody-purulent discharge. In newborn puppies, swelling and

softness of the crumbs of the paws.

Diagnosis. Symptoms of the disease are characteristic, but it is necessary to establish the main cause of its occurrence. So, with a deficiency of vitamin E, a significant number of animals suffer. Urine is usually brown. Skeletal and cardiac muscles are pale, dystrophic, subcutaneous fat is yellow or anemic.

The seasonality of the disease is expressed unsharply. A high percentage of missing females, analysis of rations and feeds indicate / an overload of diets with fat or the use of oxidized fat with insufficient supply of vitamin E. In case of feed intoxication, along with bloody urine, many or most animals show other symptoms - loss of appetite and diarrhea, and the amount patients with these signs increases not gradually, but quickly.

With urocystitis and urolithiasis, strict seasonality is characteristic (mainly July - August), male mink puppies are mainly affected, and the disease, despite some coverage of the livestock, still remains sporadic and subsides by autumn. For external stimuli (forcible capture of the animal, mating), hemorrhages in the organs of the urinary system are characteristic, which, in case of delayed emptying of the bladder, give the urine a brown color. This disease usually occurs only during the rut in the form of individual cases. Male foxes and arctic foxes are more commonly affected.

In the case of tumors, the incidence is generally single. Red paws are observed in puppies under the age of 5 days. Hereditary muscular dystrophy is differentiated using pathological and histological studies for the presence of different diameters of myofibrils in a transverse section of skeletal muscles, degenerative processes and phagocytosis of myofibrils, basophilia of their sarcoplasm, etc.

Prevention. Eliminate the main cause of the disease, most often vitamin E deficiency and feed intoxication.

urocystitis and urolithiasis(urolithiasis) - a disease predominantly of minks, characterized by inflammation of the organs of the urinary system or the formation of stones in them. Most often, mink puppies are registered in males, which differ from females in greater growth energy.

Etiology. The disease is not fully understood. It is assumed that the infectious factor plays a leading role in its etiology. After the use of antimicrobial agents at the beginning of the disease, quite satisfactory results are obtained. After infection with staphylococcus, a significant part of the minks are found to have this microbe in all layers of the stone, which also indicates an infectious etiology of the disease.

Vitamin A deficiency, if it is possible at all, is not decisive in the etiology of urolithiasis. This is confirmed by the excess content of retinol in the liver of dead animals and by unsuccessful attempts to experimentally reproduce urolithiasis in two generations of minks lacking vitamin A. Vitamin B6 deficiency is likely to be more significant.

Factors that predispose and contribute to the disease can be an intensive metabolism (the period of transition

puppies for independent food, pregnancy and lactation in females), metabolic disorders (mainly salt and nucleotide) and acid-base balance, the physico-chemical state of protective colloids that maintain salts in a dissolved state, the functional activity of the parathyroid glands, as well as stiffness water, excessive feeding of bones (calcium salts), slightly acidic or alkaline reaction of feed, poor sanitary quality of feed due to bacterial contamination, the presence of foreign toxic substances and their spoilage products.

Of the microorganisms in urocystitis and urolithiasis, Proteus, Escherichia, Staphylococcus and Streptococcus are more often isolated. They are considered the leading cause of the development of the disease (in the presence of the listed predisposing and contributing factors).

It is possible that in some cases urocystitis not only ends with urolithiasis, but is also the result of urolithiasis, since mechanical damage to the walls of the bladder ends with inflammation. Stones can get stuck in the ureters and cause blockage and, as a result, the development of hydronephrosis

or pyelonephritis.

Symptoms. Mass cases of the disease are noted in rapidly growing puppies, usually in male minks or in adult females during pregnancy and lactation. More often, the disease begins in the summer (in June - July) in mink puppies shortly after jigging. Single cases are possible at any time of the year. Symptoms of the disease are not pronounced - many patients die suddenly. The most consistent symptom is frequent urination. If the animals are taken in hand for vaccination, weighing, transplantation, treatment, then in patients they notice traces of blood or purulent exudate on the hair around the urethra, swelling in the area of ​​the frontal fusion or preputial sac. Visible mucous membranes and hairless skin (soles of the feet) are anemic, as in whiteness. In subacute or chronic course, when urolithiasis joins urocystitis, sick animals can be detected by less mobility, tense gait, paresis of the pelvic limbs, wetting, and poor appetite. Palpation can determine the presence of stones in the bladder.

Diagnosis. Find purulent or bloody discharge with urine, dysuria, paresis of the pelvic limbs, anemic visible mucous membranes, paw pads, frequent urination. A group diagnosis is made taking into account the season of the disease and the results of the pathoanatomical autopsy.

Treatment. Due to the late detection of sick animals, the effectiveness of treatment is low. Inside, antibacterial agents are prescribed - antibiotics (penicillin, neomycin, tetracycline, tetraolean, etc.) mixed with furans and sulfanilamide drugs in generally accepted dosages until recovery.

The effectiveness of treatment increases when hexamethylenetetramine is added to these drugs at 0.1-0.2 g 2 times a day or injections of ribonuclease or deoxyribonuclease at a dose of 5-10 mg in saline every other day. Positive results were obtained after the use of cystenal and urodan. Prevention. During intensive growth of young animals and reproduction of the main herd, the use of conditionally suitable and, moreover, poor-quality feed is avoided, the proportion of potentially hazardous feed that may be contaminated (contaminated) with microorganisms or toxic substances (fish meal, whole milk replacer, hydrolytic yeast, etc.) . In summer, the feed mixture must be prepared cold, at a temperature of 4 to 12 ° C, which reduces the rate of reproduction of microflora. Limit the proportion or exclude from the diet of feed with a neutral or alkaline reaction. Agents are added to the feed mixture that lower the pH and prevent the growth of bacteria: apple cider vinegar (1% to the feed in the form of a 1% solution), ortho-phosphoric acid (up to 0.5 g per 100 kcal of feed in terms of a pure preparation).

After the appearance of the first signs of disease or mortality, the entire livestock is fed 2 times a day for 7-10 days with a mixture of compatible antibacterial agents (see treatment). The course of group therapy is repeated if the incidence begins to increase again. Usually, after 2-3 courses of treatment in the summer, the mass spread of urocystitis and urolithiasis completely stops. Simultaneously with the prevention and treatment of urolithiasis, such therapy is very effective against massive gastrointestinal diseases, which often occur in the post-weaning period.

In addition to the use of antibacterial agents, they take care of the usefulness of the diet and do not allow an overestimation of the proportion of bone products and nucleic acids in it (ears, lips, milk, BVK), enrich them with vitamins and their sources (greens, nettles, etc.). In the case of an alkaline urine reaction, orthophosphoric or lactic acid, apple cider vinegar are added to the diet. The introduction of ammonium chloride, as recommended by some authors, "in our opinion, is not advisable, since the animals may have a decrease in appetite, poisoning may occur in case of an overdose of the drug, calcium salts may precipitate in the urinary organs after prolonged use with food containing excess calcium.

DISEASES OF THE SKIN

Section and dropout hair (cutting, self-cutting, flowing) is brittleness and hair loss due to metabolic disorders, stress and, possibly, hereditary pre-

location. It is observed in all types of fur-bearing animals. In some cases, when only the guard hairs are damaged, they talk about their cross section, when the guard and down hairs, they talk about a haircut. Etiology. Not finally clarified. It is assumed that the haircut is due to a deficiency of biotin, sulfur-containing amino acids, B vitamins, microelements (sulfur, copper, cobalt, magnesium). Poor quality feed and unsystematic long-term feeding of antimicrobial agents can lead to a deficiency of certain vitamins. Chronic diseases can also cause poor hair keratinization, loss of elasticity and brittleness. The cross-section is often observed even in the absence of disease, when, with a high protein content in the feed mixture, the growth of guard hairs is excessively accelerated and their strength is lost.

Cross-section and shearing, especially in certain parts of the body (on the tail, sides, sacrum, abdomen), may be the result of stress, tight manhole or hereditary predisposition.

Hair loss (weediness) occurs when some of these causes are present and as a result of a deficiency of unsaturated fatty acids or the use of feed with chemical preservatives. Post-mortem flow of hair is observed after self-heating (steaming) of carcasses of killed animals or skins removed, if they were folded tightly one to one and slowly

frozen.

When kept together in the same cage, animals can bite each other's hair, which is also due to protein deficiency and other metabolic disorders. In some animals, especially among sables, the habitual cutting or plucking of hair before whelping is sometimes noted, probably as a result of

Many defects in the quality of pubescence in some cases are hereditary, and it is very difficult to differentiate them. For example, loss of outer and downy hair on the abdomen (thinning or attrition) depends on the influence of environmental factors. So, the size of the hole in the house and the live weight of the animal are decisive in the appearance of the named anomaly.

One of the vices of fox pubescence is “samsonism”, or. "cotton fur" (sparse and short covering hair), transmitted to offspring only by females, would seem to confirm its purely hereditary origin. However, the occurrence of samsonism in healthy animals, as well as the development of normal pubescence during a new molt in former samsons, indicate a complex mechanism for the development of this pathology. Apparently, hereditary predisposition to metabolic disorders plays an important role here.

The pubescence defect in arctic foxes (felling and rubbing of hair in the rump area) largely depends on the feeding conditions, keeping, rearing method and, to a lesser extent, on

The hereditary characteristics of the animal. In foxes, a similar defect is common - bruising and splitting of hair in the sacrum, often manifested during heavy feeding.

Symptoms. On different parts of the body (tail, sacrum, back, sides or abdomen), guard hairs are devoid of ends, do not cover downy hairs. If this is observed on the body, then the hairline acquires the so-called "cotton look". When biting hair in the region of the sacrum and tail, the animals are observed, waiting for the development of self-gnawing (automutation).

Often they find animals in which all hair is bitten - both covering and downy. Moreover, the shearing zones are out of reach of the teeth of the beast, which indicates not biting, but breaking off the hair. Hair falls out before shedding, while downy hairs are also lost (the latter are depigmented in some cases). The causes of this pathology are hereditary factors (semi-lethal hairlessness). More often it is observed in puppies of individual litters and among brown minks, moreover, in the suckling or early weaning period. Alopecia is often noted in mink and ferret puppies after diarrhea. Diagnosis. They are set taking into account changes in the hairline. At the same time, hereditary semi-lethal hairlessness of brown mink puppies is excluded.

Treatment. Not developed. The use of symptomatic agents is shown: vitamins, aminopeptides, etc.

Prevention. During the laying and growth of winter hair (July - November), they strictly adhere to the recommendations for feeding, especially for protein rationing. At this time, both underfeeding and overfeeding of animals are unacceptable. Vitamin supply, diets should be reliable due to the sources of vitamins (yeast, whole fish, etc.) and concentrates (push-vit and individual vitamins). To prevent excessively rapid hair growth, the level of protein feed in the diet is somewhat lowered and grains are increased. Animals with pubescence defects are discarded.

DISEASES OF THE CENTRAL NERVOUS SYSTEM

Self-gnawing (automutation, autoaggression) is a chronic disease manifested by periodic nervous excitation, during which a sick animal gnaws certain parts of its body. Automutation (self-mutilation) occurs in fur-bearing animals in different zones, causing damage to farms due to the death of diseased animals or the deterioration of the quality of the skins. In addition, sick females often remain single, and whelping bite or jam

their puppies.

blockage of the excretory ducts of the anal glands or disturbances in the feeding of animals. Proponents of stress etiology have shown on numerous material that automutation naturally develops in most weaned puppies (for example, sables) 10-54 days after exposure to a stressor (loneliness), and without exposure to the virus and other microbiological

Among the stressors that cause the occurrence of automutation in fur animals, the following were identified: seating of weaned puppies one by one in a cage (isolation), vaccination, grading, tattooing, weighing and measuring, transplanting from place to place, exhibiting at exhibitions, transportation, fluctuations in atmospheric pressure and air temperature, noise on the farm, lack of light and sunlight, molting, violation of the feeding and hygiene regimen, inadequate diet, the presence of unauthorized persons on the farm, as well as hepatosis,

parasthesia etc.

Symptoms. Clinical signs usually appear 10-15 days after exposure to the stressor. Sables, arctic foxes and foxes get sick more often, less often minks. Thorzofretki (hybrid ferrets), characterized by almost the absence of aggressiveness, do not

The sick animal worries, spins in one place, emits a characteristic squeal, chasing its tail. Excitation attacks last a few seconds or minutes, most often occur at night or late in the evening when there are no people on the farm. A sick beast bites off hair from the tip of the tail, gnaws tissue in the region of the tip or root of the tail, anus, knee joint, paws, and sometimes the abdomen. Gradually, the animal can gnaw off the entire tail, paw or rip open the abdominal cavity, which poses a threat of death from bleeding, suppuration of wounds or peritonitis. Sometimes bite marks can only be detected upon careful examination of the animal. Attacks of self-gnawing are repeated at various intervals (3, 5, 15, 21 days or several months), in between which the patient looks clinically healthy (remission).

As the disease develops, the level of hemoglobin and erythrocytes, some enzymes decreases in the blood, the spectrum of serum proteins is disturbed, the amount of sugar and calcium increases.

and phosphorus.

In animals of many species, the disease often proceeds chronically, in foxes and arctic foxes acutely and rapidly, from 10 days to 6 months and even several years (in sables up to 5.5 years). The prognosis is often unfavorable.

Diagnosis. Set on the basis of characteristic clinical signs. Possible bites are excluded (animals inflict them on each other during mating or joint keeping in one cage), vitamin H deficiency, in which, in addition to

signs of self-gnawing, hair loss and depigmentation, dysuria, etc.

Treatment. Sick minks are injected intramuscularly with 1.5-2 ml of a 5% solution of calcium chloride and a 10% solution of calcium gluconate. The latter is used a day after the injection of calcium chloride. There is also a modification of this treatment regimen: on the first day, the sick animal is injected with 1 ml of a 5% solution of vitamin B x, on the second day - 2 ml of a 5% solution of calcium chloride, on the third day - 30 μg of vitamin B 12 . At the same time, the wounds are treated with a solution of potassium permanganate or tincture of iodine. Positive results were obtained with subcutaneous injection of 0.1% potassium permanganate solution for 3 consecutive days in doses of 1.5-2 ml for mink and sable, 2-3 ml for fox and arctic fox. However, preparations of calcium, potassium permanganate, as well as other drugs used (various ointments with ichthyol, creolin, iodoform, Peruvian balsam, iodine tincture, rivanol solutions, Dorogov's antiseptic stimulant, emulsion of streptomycin and synthomycin, hydropyrite, sulfonamides, narcotic , hypnotics and sedatives, vitamins), are not effective enough. To enhance the therapeutic effect, it is recommended to inject animals into the muscles of the croup and thigh for 3 days in a row 1-2% solution of novocaine at a dose of 0.5 ml.

In practice, combined treatment is often used: the fangs of a sick animal are first bitten with side-cutting forceps or scissors, which prevents further injury and allows you to maintain the quality of the skin, then potassium permanganate solution is injected according to the above prescription and local treatment of wounds is carried out with one of the listed antiseptics. In the event of a relapse of the disease or the ineffectiveness of the therapy, calcium gluconate, calcium chloride, novocaine, a 2.5% solution of chlorpromazine and pipolfen are additionally used (intramuscularly 2 times a day at a dose of 7-10 mg / kg for 3-4 days) .

Prevention. Do not allow single keeping of puppies from the moment of weaning from their mothers and until the time of manifestation of their quarrelsomeness with each other (until the end of July - beginning of August). This is especially true for excitable sables. They limit the holding of activities related to catching animals, violation of the daily routine, do not allow unauthorized persons to farms, monitor the correct feeding and maintenance of animals. Sick females, along with their puppies, are culled and removed from the herd, and after the maturation of the hairline, they are killed to obtain the skin. Sick puppies are culled.

test questions

1. Peculiarities of respiratory diseases in fur-bearing Evereyes; diagnostics,
prevention and treatment of rhinitis.

2. Etiology, diagnosis and treatment of bronchopneumonia.

3. Symptoms, treatment and prevention of stomatitis and gastroenteritis.

4. Etiology, diagnosis and therapy in acute gastric distention and
blockage of the intestine.

5. Etiology, diagnosis and prevention of mink hepatosis.

6. Clinical features and prevention of hypovtaminoses AT% and V a.

7. Lactational exhaustion of females, diagnosis and prevention.

8. Methods of diagnosis, treatment and prevention of iron deficiency
anemia.

9. Differential diagnosis of dysuria and hematuria, prophylactic methods
tics and therapy.

10. Etiology, diagnosis and control of urocystitis and urolithiasis
disease.

11. The main symptoms of splitting and hair loss in sables and minks,
prevention methods.

12. Causes of self-nibbling in animals, methods of diagnosis, prevention

and therapy.

CONTENT

Foreword ................................................................ ................................................. ...

3
Introduction ................................................ ................................................. ............ B

General prevention and therapy of internal non-communicable diseases of the abdomen
nykh (V. M. Danilevsky).................................................. ............................................ 12

Prevention planning (12). Medical examination
tion (14). Principles of veterinary therapy (18). Means veterinarian
therapy (21). Methods of veterinary therapy (22). diet therapy
(thirty). Preventive and therapeutic measures in animal husbandry
ski complexes and specialized farms of industrial
type (32).
43

Methods and means of physiotherapy and physioprophylaxis (L. M. Obukhov) 45

Light therapy (phototherapy) .............................................. ................................. 45

Infrared radiation (46). Ultraviolet radiation (50). The use of solar radiation in the treatment and prevention of diseases (55).

Electrotherapy ................................................................ ................................................. ..56

Galvanotherapy (56). Electrophoresis (58). Electrotherapy with impulse currents of low frequency and voltage (59). Darsonvalization (60). Inductothermy (62). Microwave therapy (63). Ultrahigh frequency therapy (64).

Ultrasound therapy .................................................................. ............................................... 66

Aeroionotherapy .............................................................. ............................................. 68

Protective measures during electrotherapy .............................................................. ........ 69

Mechanotherapy (mototherapy) .............................................. ............................... 70

Hardening of the animal body .................................................................. ................. 71

Test questions................................................ ......................................... 72

Methods and means of therapeutic technique (A. V. Korobov) .............................. 73

The main methods of fixing animals and safety precautions when providing
Help .................................................................. ................................................. .................... 73

Methods of drug administration .................................................................. ............ 75

Voluntary methods (75). Violent methods (75).

Probing and lavage of the proventriculus and stomach .............................................. 85

Metal indication and insertion of magnetic probes and rings into the proventriculus 91

The use of enemas .............................................................. ................................................. 92

Bladder catheterization and lavage ............................................................... ... 95

This book is the first fundamental veterinary work in fur farming for many years and is intended primarily for practitioners. It most fully outlines the issues of the pathology of carnivorous fur-bearing animals - farm foxes, arctic foxes, sables, minks and raccoon dogs. Many information about diseases and veterinary problems, mined bit by bit over decades by scientists and practitioners, incl. and the author, are considered in detail and generalized, based on modern ideas, due to which they will become the prerogative or "know-how" of not individual specialists, but all readers. A number of diseases, the danger of which was previously exaggerated or underestimated, are described here in a new way. The chapters covering contagious diseases of animals provide information on susceptible agricultural and wild animals (birds) and the possibility of infection of humans and fur-bearing animals from these animals and vice versa.
The author of the book is V.S. Slugin, Honored Veterinary Doctor of the RSFSR, laureate of the Prize of the Government of the Russian Federation, Doctor of Veterinary Sciences, who has been working in fur farming for almost 50 years, incl. 32 years as a practical veterinarian in fur farms, knows firsthand the pathology of animals and from the bottom of his heart gives readers his medical secrets.

The book is intended for specialists in animal husbandry, animal husbandry, researchers, teachers, students, as well as for physicians.

The file will be sent to selected email address. It may take up to 1-5 minutes before you receive it.

The file will be sent to your Kindle account. It may take up to 1-5 minutes before you receive it.
Please note you "ve to add our email [email protected] to approved email addresses. Read more.

You can write a book review and share your experiences. Other readers will always be interested in your opinion of the books you "ve read. Whether you" ve loved the book or not, if you give your honest and detailed thoughts then people will find new books that are right for them.

-- [ Page 1 ] --

INFECTIOUS DISEASES

FUR ANIMALS

(MONOGRAPH)

VITEBSK, 2008

veterinary sciences, professor

worker of science of the Republic of Belarus;

Prudnikov V.S. – Doctor of Veterinary Sciences, Professor of the Department of

tological anatomy and histology of the MA VGAVM;

Karasev N.F. – Doctor of Veterinary Sciences, Professor of the Department of Para-

zitology and parasitic diseases UO VGAVM;

Nikolaenko M.F. - Assistant of the Department of Diseases of Small Animals and Birds of UO VGAVM.

Reviewers: Medvedev A.P. - Doctor of Veterinary Sciences, Professor of the Department of Microbiology and Virology, UO VGAVM;

Olekhnovich N.I. – Candidate of Veterinary Sciences, Associate Professor of the Department of Zoology, UO VGAVM.

Yatusevich A.I., Prudnikov V.S., Karasev N.F., Nikolaenko M.F.

Infectious diseases of fur animals Monograph / A.I. Yatusevich, V.S.

Prudnikov, N.F. Karasev, M.F. Nikolaenko. - Vitebsk: UO VGAVM, 2008. 110 p.

The manual is intended for veterinary workers and students of the faculty of veterinary medicine.

Reviewed and approved at a meeting of the educational and methodological commission of the Faculty of Veterinary Medicine (Minutes No. 2007) Approved for publication by the editorial and publishing council of the Vitebsk Order of the Badge of Honor State Academy of Veterinary Medicine

Protocol No. UDC: 619:616.9:636. LBC: 48. © A.I. Yatusevich and others, © UO "Vitebsk Order of the Badge of Honor"

State Academy of Veterinary Medicine, CONTENTS Page.

Introduction 6- Diseases of bacterial etiology 1. Escherichiosis 2. Salmonellosis 3. Pasteurellosis 4. Streptococcosis 5. Staphylococcosis 6. Pseudomonosis 7. Leptospirosis 8. Botulism 9. Tuberculosis 10. Chlamydia 11. Dermatophytosis (microsporia, trichophytosis) 35- Diseases of viral etiology 12 Canine distemper 13. Parvovirus enteritis 14. Infectious hepatitis 15. Canine adenovirus infection 16. Rabies 17.

Due to a number of features, infectious diseases are the most dangerous group of diseases that exist in nature as a result of the continuity of the epizootic process and are capable of causing great economic damage to fur farming under certain conditions, and some of them are also dangerous for humans.

Diseases of contagious etiology occupy a large place among all known diseases. Clinical manifestation, treatment and prevention are of no small importance in infectious diseases.

The monograph in an accessible form covers the issues of etiology, pathogenesis, clinical manifestations of infectious diseases of various etiologies in fur-bearing animals. The issues of their treatment and prevention are described.

Bacteriosis of fur animals Escherichiosis (echerichiosis) is an infectious disease accompanied by profuse diarrhea, signs of severe intoxication and dehydration.

Etiology. The causative agent of the disease is enteropathogenic strains of E. coli, which are characterized by high virulence and hemolytic properties. The causative agent of the disease, a facultative anaerobe, is a short, thick (0.2–0.7 x 2–4 µm), Gram-negative bacillus with rounded ends that does not form spores or capsules.

The causative agent in feces and excreted exudate retains its biological activity for up to 30 days, in soil, water - up to several months.

Epizootology. A newborn young nymph at the age of 1–4 days is susceptible to the disease, somewhat less often at 5–10 days of age.

The source of the infectious agent is sick and recovered animals, as well as adults - bacteria carriers, intensively excreting the pathogen with feces, and sometimes with urine.

The pathogen transmission factors are infected feed, water, inventory, bedding, overalls, etc. The carriers are wild rodents and birds.

Infection occurs both during childbirth, in particular, when the rules of hygiene are not observed, and when the conditions for feeding and keeping animals are violated. The pathogen enters the body with food, water, less often aerogenic.

The disease proceeds in the form of enzootics, covering a significant number of animals, without a strictly pronounced seasonality. In stationary disadvantaged farms, the lethality of puppies can reach 15–25%.

Pathogenesis. Enteropathogenic strains of the pathogen, once in the gastrointestinal tract, cause the development of dysbacteriosis and the phenomenon of intoxication. Later, penetrating into the bloodstream, they cause the state of septicemia.

Symptoms and course. The incubation period lasts 1-5 days and is characterized by acute and subacute course. In puppies, the disease manifests itself in enteritis and septic forms.

In the enteric form, a decrease in appetite is noted, the puppies become inactive, restless, and squeak. Signs of inflammation of the gastrointestinal tract develop - the feces become liquid, mushy, yellow in color. In the future, diarrhea intensifies, the color of the excrement becomes gray-white or dark gray with an admixture of mucus, a fetid odor, sometimes the feces foam. In suckling puppies, the feces contain clots of curdled milk, sometimes with an admixture of blood. In severe cases, the act of defecation is accelerated and becomes involuntary. The coat near the anus, on the tail, on the hind limbs is damp, contaminated with dried, sticky stools. Body temperature at the onset of the disease reaches 40.0–41.5 °C, during the agonal period it drops to normal and even lower. The puppies are rapidly losing weight, the fur loses its luster, becomes disheveled, movement coordination is disturbed due to the weakness of the hind limbs (Fig. 1). In an acute course, the disease ends with death on the 3-6th day. With substrom - for 10-16 days.

Rice. 1. A mink puppy with an enteric form of escherichiosis.

The septic form is accompanied by symptoms of meningoencephalitis, the development of dropsy of the brain (Fig. 2), with impaired coordination of movement, the development of paresis and paralysis of the limbs, and convulsions.

Fig.2. A polar fox puppy with escherichiosis.

Dropsy of the brain. coma.

In infected pregnant females, abortions or stillbirths of puppies, loss of appetite and depression are recorded.

In nutria puppies, the earliest sign of illness is restlessness, expressed in a continuous squeak. The hairline and skin near the anus are contaminated with feces. With a light massage of the abdomen, liquid feces of an inhomogeneous consistency, yellow-green or white-yellow in color with bubbles of gas and mucus, are released from the anus.

pathological changes. At the autopsy of corpses that fell from escherichiosis, they reveal:

- enlargement of the spleen (splenitis);

- catarrhal-hemorrhagic enteritis, in some cases with hemorrhages on the mucous membrane;

- serous lymphadenitis of the mesenteric nodes;

- exicosis.

Diagnosis. The diagnosis of escherichiosis is established on the basis of clinical and epizootological data, the results of pathoanatomical changes with the obligatory microbiological changes.

The diagnosis is considered established when Escherichia cultures are isolated from the following two organs: spleen and bone marrow or spleen and brain without determining pathogenicity and serological affiliation.

In addition, the diagnosis will be recognized as having been established upon isolation of at least two organs of Escherichia pathogenic for white mice.

Escherichiosis should be differentiated from viral gastroenteritis, salmonellosis, eimeriosis, gastroenteritis of non-contagious etiology and streptococcosis.

Treatment. As a specific treatment, polyvalent antitoxic serum against salmonellosis and escherichiosis of farm animals and birds is used. In addition, the means of pathogenetic, symptomatic and rehydration therapy are used. Antibacterial drugs are used only after determining their sensitivity to the isolated cultures of Escherichia.

Prevention and control measures. When establishing a diagnosis, restrictions are introduced, under the conditions of which a thorough clinical examination and thermometry are carried out, followed by isolation and treatment of sick animals.

Carry out disinfection of enclosures, sheds, houses, inventory using a 2–3% hot solution of sodium hydroxide or formal dehyde;

3% chloramine solution or 2% hypochlorine solution;

1% solutions of virkon C, polysept, metacid, fogucid.

Females are immunized in order to create passive immunity in puppies, using a polyvalent vaccine against salmonellosis and escherichiosis of fur animals. They create an optimal technological regime for keeping animals. Carry out decontamination. The corpses of dead animals are destroyed. Manure is disinfected biothermally.

Restrictions are removed in the absence of sick animals, obtaining a healthy offspring and implementing veterinary and sanitary and special measures in full.

Salmonellosis (salmonellosis) is an infectious disease of young animals, characterized by dysfunction of the digestive tract, the development of sepsis, sometimes metritis and abortion in adult animals.

Etiology. The causative agent of the disease is a gram-negative movable rod with rounded ends, it does not form spores and capsules, and is relatively stable in the external environment. The disease in small animals is more often caused by Sal. cholerae suis, Sal. enteritidis, Sal. typhi murium.

Epizootology. Young animals of all types of domestic and farm animals are susceptible to salmonellosis. Carnivores often get sick at the age of 1-6 months, rabbits and nutria at 1-3 months of age.

The source of the infectious agent is sick animals and bacteria carriers that excrete the pathogen with feces, urine, nasal discharge, saliva and milk. Transmission factors of the pathogen are infected feed (meat and bone and fish meal, slaughterhouse waste), in addition, water, bedding, care items. Mice, rats, birds, insects can be carriers of the pathogen.

Infection occurs in an alimentary way. Perhaps aerogenic and intrauterine infection. Outbreaks of the disease are recorded at any time of the year, in the presence of a susceptible contingent of animals. The disease is characterized by stationarity, with the intensive development of epizootics with a wide coverage of a large number of animals.

Pathogenesis. Salmonella, once on the intestinal mucosa, actively multiply, releasing exo- and endotoxins, causing inflammation. With insufficient resistance of the organism, septicemia develops with characteristic clinical signs.

Symptoms and course. The incubation period for carnivores is 3–20 days, for rabbits and nutria 2–5 days. The course of the disease is acute, acute and chronic.

In carnivores, in the acute course of the disease, an increase in body temperature, lethargy, and a decrease in appetite are recorded. Vomiting is often noted (especially after eating), convulsions are sometimes observed with the release of foam from the mouth. Then diarrhea develops, while the feces have a fetid odor and contain a large amount of mucus and blood. Puppies quickly lose weight, the hairline near the anus becomes contaminated with feces. Death occurs on the 2-3rd day.

In rabbits and nutria, food refusal is noted, a short-term excitation, which turns into a coma. The body temperature rises to 41–42 °C. Sometimes there is vomiting and diarrhea. In nutria, in addition, bloody discharge from the nose, convulsions, paralysis of separate pectoral muscles, weakness of the backside and profuse salivation are recorded.

In subacute course, along with signs of pathology of the gastrointestinal tract, carnivores have a respiratory disorder with the development of bronchopneumonia and purulent discharge from the nose.

Breathing becomes difficult, and wheezing is heard in the lungs. Sometimes nervous phenomena appear, aggressiveness increases.

In the case of the development of toxic infection, regardless of the type of animal, the disease is accompanied by a temporary disorder of the functions of the gastrointestinal tract.

pathological changes. When opening the corpses of animals, with an acute course of the disease, they find:

- hemorrhages in the internal organs, on the serous and mucous membranes;

– enlargement of the spleen by 5–8 times;

- granular and fatty degeneration of the liver with foci of necrosis;

- serous pleuropneumonia;

in subacute course - catarrhal bronchopneumonia.

Diagnosis. The diagnosis of salmonellosis is established taking into account a complex of clinical and epizootological data, autopsy results and laboratory tests. Intravital diagnosis is based on the study of fecal and blood samples.

Salmonellosis should be differentiated from alimentary gastroenteritis, escherichiosis, pasteurellosis, streptococcosis, infectious hepatitis, which is based on the isolation of the pathogen and serological identification.

Treatment. Treatment should be complex, involving the use of etiotropic, pathogenetic, symptomatic therapy. Antibacterial preparations should be used taking into account the sensitivity of Salmonella to them. Of the specific agents, in the treatment of animals with salmonellosis, polyvalent antitoxic serum is used.

Prevention and control measures. The effectiveness of health-improving measures for salmonellosis is determined by the degree of implementation of a set of measures, including the isolation of sick animals, their treatment;

timely implementation of forced disinfection, which provides for breaking the epizootic chain and preventing further spread of the infectious agent;

immunization of clinically healthy animals. In order to create immunity in livestock, a polyvalent vaccine against salmonellosis and escherichiosis of fur-bearing animals is used. Mandatory measures are provided for the implementation of deratization and disinfection of equipment, care items, overalls;

disposal of manure and feed residues;

burning corpses;

quarantine of newly arrived animals.

For disinfection, a 3% solution of sodium hydroxide, a 2% solution of formaldehyde, 1% solutions of metacid, polysept, foguni yes, virkon S should be used.

Carcasses of forcedly slaughtered rabbits and nutrias, with good fatness, are used for food after 1.5 hours of boiling. Exhausted - disposed of.

A dysfunctional farm (fur farm) is considered recovered from salmonellosis 3 months after the recovery of sick animals, vaccination and final disinfection.

Pasteurellosis (hemorrhagic septicemia) is an infectious disease of many animal species, characterized by signs of septicemia and hemorrhagic inflammation of the mucous membranes of the respiratory tract and intestines, in a chronic course, complicated by pneumonia, otitis, subcutaneous tissue abscesses.

Etiology. The causative agents of the disease are gram-negative bacteria: P. multocida and P. haemolytica (which do not show pathogenic properties against white mice and rabbits, are resistant to neomycin). Pasteurella, in smears-imprints from organs and blood, stained with Leffler's blue, have the appearance of bipolar and are short rods arranged singly or in pairs. Bacteria are immobile, do not form spores, highly virulent strains form a capsule, a facultative anaerobe.

The stability of Pasteurella is not high - they remain in corpses for up to 4 months, in manure - up to a month, at a temperature of 70–90 0С, inactivation occurs after 10 minutes.

Epizootology. Puppies of fur-bearing animals and rabbits are most susceptible to pasteurellosis, puppies of dogs are somewhat less likely to get sick.

The source of the infectious agent is sick and recovered animals, as well as Pasteurella carriers, which release bacteria into the external environment with expiration from the nose, with exhaled air, saliva, feces and urine. Among Pasteurella-carriers (there are up to 50% of them in the herd), the greatest danger is posed by animals that secrete virulent strains of Pasteurella. The disease can manifest itself as a secondary infection against the background of the main - dominant one.

The transmission factors of the pathogen are poultry meat infected with Pasteurella, offal fed to animals in a non-decontaminated form. In addition, infected care items, bedding, wool, water, air, overalls and shoes play an important role in the occurrence of the disease. Carriers of pathogens can be wild rodents, blood-sucking insects, pigeons and poultry, which are a permanent reservoir of pathogens.

Infection occurs mainly through the digestive tract and respiratory tract, infection through damaged skin upon contact with sick animals and mucous membranes is possible.

There is no clear seasonality, but epizootics are more often recorded in spring and autumn. Often, after half a year, repeated outbreaks of the disease are observed, which can be explained by the circulation of pathogenic strains of Pasteurella in the external environment and which ensures the formation of stationary epizootic foci.

The incidence of pasteurellosis is 50-80%, mortality - 80-95%.

Pathogenesis. Virulent strains of Pasteurella actively multiply at the sites of introduction, and then penetrate into the bloodstream, causing septicemia. The toxins produced by them increase the porosity of blood vessels, resulting in hemorrhages, pulmonary edema, and pneumonia.

Symptoms and course. The incubation period lasts from 5 hours to 3 days. The disease proceeds superacutely, acutely and chronically. In a hyperacute course, patients die suddenly, without any characteristic clinical signs.

Pasteurellosis in fur-bearing animals, as a rule, proceeds acutely and is manifested by sharp oppression, refusal to feed, shaky, uncertain gait, and vomiting. Visible mucous membranes are cyanotic (yellow in foxes).

In the future, diarrhea appears, sometimes blood is found in the feces. Most often, the phenomena of hemorrhagic gastroenteritis are recorded in silver-black foxes. At the same time, an increase in body temperature to 41.8–42.5 ° C, foamy discharge of exudate from the nose and mouth, rapid and difficult breathing are noted.

In nutria, pasteurellosis often occurs acutely and is accompanied by loss of appetite, depression, lacrimation and salivation, and vomiting. The body temperature rises to 40.5 °C, ruffled coat, labored and rapid breathing, diarrhea, paralysis of the hind limbs are observed.

The main symptom of nutria pasteurellosis is epistaxis, which appears shortly before the death of animals.

In rabbits with an acute course of the disease, the body temperature rises sharply to 41–42 ° C, they are depressed, breathing is shallow, rapid. Rhinitis, sneezing, diarrhea are observed, and after 1–3 days the animals die.

In a chronic course, rhinitis is expressed, accompanied by the release of purulent exudate and blockage of the nasal passages. develops conjunctivitis. In some cases, purulent-fibrinous pneumonia, otitis media and abscesses in the subcutaneous tissue of different parts of the animal body are recorded.

pathological changes. In an acute course, in carnivores, they find:

- hemorrhagic diathesis;

- granular dystrophy of the liver with overflow of the gallbladder with thick dark green bile;

- granular dystrophy of the kidneys with foci of necrosis;

- enlargement of the spleen;

- catarrhal-fibrinous pneumonia (in dogs);

- serous-hemorrhagic lymphadenitis;

foxes have jaundice.

Diagnosis. The diagnosis of pasteurellosis is made on the basis of epizootological analysis, clinical signs and pathoanatomical changes with mandatory bacteriological examination with the establishment of pathogenicity in the isolated culture of the pathogen.

Pasteurellosis must be differentiated from Aujeszky's disease, plague, streptococcosis, in minks from botulism.

Treatment. Serum against pasteurellosis of pigs, rabbits and fur-bearing animals is used as a specific agent. Antibacterial drugs are used after determining their sensitivity to the isolated culture of the pathogen.

Prevention and control measures. In order to prevent the occurrence of pasteurellosis, an important factor is the strict observance of general preventive measures, as well as veterinary and sanitary rules and preventive vaccination.

When establishing a diagnosis, restrictions are introduced. At the same time, the import, export, regrouping of animals and the performance of surgical operations are prohibited.

After conducting a clinical study, animals are divided into groups: sick and suspicious of the disease - isolated and treated;

those ripened in infection are vaccinated. In order to create an active immunity to them, a formol vaccine against pasteurellosis in rabbits is used. For vaccination of nutrias and minks, an emulsified vaccine is used. In addition, for the immunization of animals, a bivalent saponin formol hydroxide-aluminum vaccine against streptococcosis and nutria paste rellosis, as well as an associated vaccine against botulism and mink paste terellosis are used.

The bodies are burned or disposed of.

The carcasses of forcedly killed rabbits are used for food after an hour of boiling, and the internal organs are destroyed. The skins are treated from the side of the mezra with a 1% solution of phenol or formalin.

Deratization and forced disinfection are carried out using a 20% suspension of freshly slaked lime, hot 2% sodium hydroxide solution, 0.5% formaldehyde solution.

Restrictions on the farm are removed 14 days after the last case of the disease, immunization of susceptible livestock and the implementation of the entire complex of veterinary and sanitary measures, including final disinfection.

Streptococcosis (streptococcosis) is an acute infectious disease characterized in acute course by sepsis and inflammation of the joints, in subacute and chronic inflammation of the lungs and intestines. In adult animals, the disease is manifested by abortions, postpartum mastitis and endometritis.

Etiology. The causative agent of the disease is pathogenic beta-hemolytic streptococcus, belonging to group C of the genus Streptococcus, species Str.

pneumoniae (Dipl. septicum, Dipl. lanceolatus). In smears from the pathological material, a capsule is detected, and the pathogen is located in pairs or in short chains, it stains gram-positively. The size of cocci is 0.5–1.5 microns, they are immobile, do not form spores, facultative aerobes.

In the soil, manure and indoors, streptococcus persists for 3 weeks, in dried blood and sputum - up to 2 months, heating to 55 ° C inactivates the pathogen in 30–45 minutes.

Epizootology. The most susceptible to the disease are sables and silver-black foxes of all ages. Arctic foxes, minks, nutrias, rabbits, and dogs are more resistant. More often, the disease is recorded in young animals from up to 70 days.

The source of the causative agent of infection are sick and recovered from streptococcosis animals. The pathogen is excreted from the body with nasal and vaginal discharges, urine and feces.

The transmission factors of the pathogen are infected food, milk, water, inventory, bedding. Infection of animals occurs by alimentary and aerogenic routes. The disease is more common in the autumn-winter period. Morbidity is 30-50%, mortality reaches 70-90%.

Pathogenesis. When the pathogen enters the mucous membrane of the respiratory tract and digestive tract, it quickly penetrates into the blood, suppresses phagocytosis and causes septicemia. The released exotoxins destroy the vascular endothelium, increase their porosity, thereby causing abundant hemorrhages on the serous and mucous membranes.

Symptoms and course. The incubation period is 3–7 days. The course of the disease is hyperacute, acute, subacute and chronic. Disease forms: septic (40.1%), pulmonary (26.4%), intestinal (24.8%), nervous (8.7%).

The hyperacute course is characterized by signs of septicemia and intoxication. The disease begins suddenly and is accompanied by depression, fever, conjunctivitis, rhinitis, and the release of foamy exudate from the nasal cavity. Death occurs within a few hours with symptoms of pulmonary edema.

Fig.3. A fox puppy with streptococcosis.

Swelling of the joint of the left leg.

In an acute course, puppies refuse food, become lethargic, inactive. There is an increase in body temperature up to 40 0C, sometimes vomiting, bloody outflows from the nasal openings, diarrhea appear, joints are often affected (Fig. 3) and nervous phenomena are noted (Fig. 4).

In minks, streptococcosis in most cases occurs in the form of abscesses in the neck and head. In addition, the main symptoms of the disease are: pneumonia, endocarditis, peritonitis, which leads to the development of sepsis. Sometimes signs of damage to the nervous system are recorded in the form of impaired coordination of movements, periodically recurring tonic convulsions are noted.

Rice. 4. A fox puppy with streptococcosis.

nervous phenomena.

Pregnant females may have abortions in the second half of pregnancy (up to 8%), the birth of defective puppies, metritis.

In rabbits with streptococcosis, underdeveloped rabbits are born. There are abortions in the second half of pregnancy. In some rabbits, semi-paralysis of the muscles of the pelvic girdle and hind limbs is noted.

pathological changes. When opening the corpses of dead animals, they reveal:

in rabbits: catarrhal-hemorrhagic gastroenteritis with pinpoint hemorrhages on serous and mucous membranes;

- gelatinous infiltration of subcutaneous tissue in the pharynx and trunk;

- pulmonary edema;

- hyperplasia of the spleen and lymph nodes;

- liver dystrophy;

in dead dogs

- catarrhal-purulent mastitis;

- urocystitis, endometritis, vaginitis;

puppies of fur-bearing animals have signs of septicemia.

Diagnosis. The diagnosis is established taking into account epizootological data, clinical signs, pathoanatomical changes and the results of bacteriological studies with the establishment of the presence of pathogenic properties in the isolated culture of the pathogen.

Streptococcosis must be differentiated from salmonellosis, pasteurellosis, escherichiosis, Aujeszky's disease, plague, pseudomonosis and gastroenteritis of non-contagious etiology.

Treatment. Hyperimmune serum against streptococcosis is used as a specific treatment. Carry out symptomatic treatment.

Prevention and control measures. In order to prevent disease on farms, the veterinary and sanitary regime of closed enterprises must be observed. At the same time, it is strictly forbidden to import animals, feed, cages, etc. from farms that are unfavorable for streptococcosis.

When the diagnosis is established, the farm (farm) is declared unfavorable and restrictions are introduced. Clinical investigations are carried out daily, and sick and suspected patients are isolated and treated.

The premises are disinfected with a 2% formaldehyde solution, a 1% solution of Virkon C and a hypochlorine solution containing 2% active chlorine.

Organize the extermination of wild rodents, scare away birds, stray dogs and cats.

Manure, bedding is removed daily and subjected to biothermal disinfection. Inventory of little value is burned.

All clinically healthy animals are vaccinated, in particular, for nutria, a saponin-aluminum hydroxide vaccine against pas terellosis and streptococcosis is used.

Corpses and fat, after skinning, are burned.

Restrictions on a dysfunctional farm are removed 15 days after the last case of recovery or slaughter of animals. Carry out final disinfection.

Staphylococcosis (staphylococcosis) (staphylococcal pyoderma of newborn mink puppies, staphylococcal dermatitis) is an acute infectious disease manifested by suppurative processes in various tissues.

Etiology. The causative agent of the disease, Staphylococcus pyogenes aureus, has a characteristic morphology for this group of microbes: it does not form spores and capsules, is immobile, is located in the form of grape clusters, spherical in shape, 0.7–1.0 μm in diameter, gram-positive aerobe, actively reproduces on ordinary nutrients. environments.

Epizootology. All types of fur animals are susceptible to the disease, especially mink puppies in the first days of life.

The source of the causative agent of infection are female carriers, as well as sick puppies of the same litter. The causative agent enters the external environment with purulent exudate during the opening of abscesses. Transmission factors of the pathogen are infected litter, cages, feed, care items.

Infection occurs through damaged skin and mucous membranes. This can happen while the female is massaging the puppy's belly with her tongue or while dragging the puppies, when the female grabs him by the skin of the neck. Contributing factors are: unsanitary conditions of keeping animals, the presence in the cells of sharp, prickly objects (nails, wire) leading to skin damage.

There is no pronounced seasonality in the manifestation of enzootics, but most often the disease is recorded during the appearance of puppies. Stationarity is characteristic of pyoderma due to the wide distribution of the pathogen and the presence of microcarrier animals.

Pathogenesis. Penetrating into the tissues of the animal, staphylococci cause a purulent inflammatory reaction, which, when a massive dose of the pathogen is received, can proceed in the form of severe septicemia.

Symptoms and course. In mink puppies, the incubation period lasts 24–48 hours. Sick puppies weaken, lag behind in growth. Very small abscesses appear in the thickness of the skin, on the dorsal side of the neck and in the perineum, which merge, reaching the size of a pea.

When they are opened, thick yellow-green pus flows out.

In some cases, the affected areas are dark red with a purple tint, without the presence of abscesses, which is an indicator of a severe course of the disease. Among puppies 1-2 days of age, mortality is high, puppies older than 4 days of age get sick much easier.

In the case of the development of wandering (vagrant) pyemia under the skin of the lips, head, back, lateral surface of the body, characteristic fluctuating abscesses ranging in size from a pea to an apple are found, and sometimes protrusion of the eyes is recorded due to the formation of an abscess behind the eyeball.

pathological changes. The autopsy of the dead animals allows us to state the presence of abscesses, purulent urocystitis, pyelonephritis and catarrhal-hemorrhagic gastroenteritis.

Diagnosis. The diagnosis is established on the basis of clinical and epidemiological data, laboratory results. In the process of diagnosis, streptococcosis, pasteurellosis should be excluded, in rabbits - myxomatosis.

Treatment. The affected areas of the skin are wiped with a 5% solution of salicylic alcohol or treated with an ointment consisting of 5 g of salicylic acid, 10 g of tannin and 85 g of petroleum jelly. Subcutaneous abscesses are surgically removed along with the capsule, treated with antiseptic agents, followed by suturing. Weak puppies are injected subcutaneously with hydrolyzate, glucose, vitamins, antibiotics.

With an abscessing form, the abscess cavity is opened, freed from the contents and treated with a 3% hydrogen peroxide solution. The wound is sprinkled with streptocide, tricillin and Vishnevsky's liniment is applied.

Antibiotics are injected intramuscularly.

Prevention and control measures. Prevention of the occurrence of the disease is mainly based on maintaining optimal conditions for keeping animals, ensuring a high level of body resistance;

timely and high-quality implementation of veterinary and sanitary measures;

identification and isolation of sick animals with their subsequent treatment;

culling of sick animals and puppies in this litter.

In the event of a disease, a thorough current disinfection is carried out, and at the end of the outbreak, the final one. In stationary disadvantaged farms, where there are real conditions for the occurrence of pyoderma, it is recommended that females be immunized with staphylococcal toxoid. It is administered twice at a dose of 0.5 ml on the 10-12th and 15-17th day of pregnancy.

Mink pseudomonosis is an acute contagious disease accompanied by hemorrhagic pneumonia, septic phenomena, and high mortality.

Etiology. The causative agent of the disease is Pseudomonas aeruginosa, motile (monotrich), short, Gram-negative, 0.8–1.4 x 0.4–0.6 µm in size. The spore does not form, aerobe, when cultivated on dense nutrient media, forms S-shaped colonies, which is an indicator of the high virulence of the strain. The causative agent belongs to conditionally pathogenic microflora and can be isolated from healthy animals.

Epizootology. Minks are most susceptible to pseudomonosis, although the disease has been recorded in other animal species, in particular, in young arctic foxes.

The source of the infectious agent is sick animals that excrete the pathogen into the external environment with bloody discharge from the nasal cavities, as well as when coughing and sneezing, with urine and feces.

The transmission factors of the pathogen are infected meat and fish feed, cottage cheese (made from the milk of a cow with mastitis), as well as water, equipment, fluff and wool.

Infection occurs by alimentary and aerogenic routes. Wild rodents can be a reservoir of the pathogen, contributing to long-term ill health.

The disease most often occurs in the summer-autumn period. However, sporadic cases can occur at any time of the year.

The incidence of young minks can range from 18 to 50%, and the mortality rate is 40–50%. In adults, mortality is only 5–7%.

Pathogenesis. After introduction into the body, with the blood flow, the pathogen penetrates into the lungs, where it multiplies intensively, causing the development of hemorrhagic inflammation and sepsis. The permeability of blood vessels increases, and petechial hemorrhages appear on the serous and mucous membranes.

Symptoms and course. The incubation period, with experimental infection, is 10–18 hours, with natural infection, 2–5 days.

The disease proceeds superacutely and acutely. The characteristic symptoms of the disease appear 1.5–2 hours before death in the form of bloody-foamy outflows from the nasal openings and nasal cavity;

difficulty breathing and wheezing.

The death of animals occurs with increasing signs of asphyxia.

In addition to minks, blue fox puppies at the age of 2–2.5 months suffer from Pseudomonosis, in which diarrhea is recorded, accompanied by the release of feces of a liquid consistency, an unpleasant odor.

In females, shortly before whelping, abortions occur.

pathological changes. When opening fallen minks, they reveal:

- catarrhal-hemorrhagic enteritis;

- hemorrhagic pneumonia (or pulmonary edema), the presence of bloody exudate in the trachea and bronchi;

- hyperplasia of the spleen.

Diagnosis. The diagnosis is established on the basis of clinical, epidemiological data, the results of a pathoanatomical autopsy with mandatory microbiological studies of the pathological material.

The determining factor is the isolation of the culture of the pathogen and the establishment of its virulent properties.

Pseudomonosis must be differentiated from pasteurellosis, salmonellosis, plague, Aleutian disease, etc.

Treatment. The effectiveness of the treatment of sick animals depends on the stage of the infectious process and the selection of antibacterial agents. As specific means of treatment, serum and immunoglobulin are used with the simultaneous use of drugs for etiotropic, pathogenetic, symptomatic therapy, as well as agents that stimulate the protective properties of the body.

Prevention and control measures. When a diagnosis is established, quarantine is introduced, under the terms of which strict measures are taken to stop the source of infection.

A clinical study is carried out daily, followed by isolation and treatment of sick and suspicious animals. The rest of the animals are vaccinated. In order to create active immunity, 2 3-month-old minks are immunized with a polyvalent formol aluminum hydroxide vaccine against pseudomonas. In addition, an associated vaccine against viral enteritis, botulism and pseudomonas is used;

associated vaccine against enteritis, botulism, pseudomonosis and canine distemper.

They organize the extermination of rodents, scare away wild birds and take measures to exclude the entry of dogs, cats and other animals into the farm.

The cage where sick animals were kept is disinfected using a 2% hot solution of sodium hydroxide or formalin, or a solution of bleach (containing 2% active chlorine), or a 1% solution of Virkon C.

Manure, bedding and food residues are destroyed, a wide range of veterinary and sanitary measures are carried out.

Organize daily sanitation of overalls, inventory, care items. The corpses are burned after skinning.

Restrictions are lifted after 15 days from the date of the last case of the death of animals and the implementation of all veterinary and sanitary measures.

Leptospirosis (leptospirosis) is an infectious natural focal disease, manifested by short-term fever, hemoglobinuria, ulcerative stomatitis, hemorrhagic gastroenteritis, anemia, jaundice, necrosis of the mucous membranes and skin, nervous disorders.

Etiology. The causative agent of the disease belongs to the genus Leptospira, which includes the following serogroups: L. canicola, L. icterphaemorrhagia, much less often L. pomona.

Morphologically and culturally, leptospira of different serovars are identical and look like delicate, thin, spiral rods and filaments, with hooked ends, with active movement, 7–14 µm long. Leptospira are cultivated on liquid elective nutrient media of Ulengut, Lyubashenko, Tersky, including 5–10% rabbit or mutton serum. In the water of rivers, lakes and ponds, leptospira remain viable for up to 100 days, in soil - up to 280 days, in fresh urine - up to 4-7 days. Withstand freezing.

Epizootology. Leptospirosis affects silver-black foxes, dogs, arctic foxes, raccoons, minks and cats, less often rabbits and nutrias, humans are also susceptible.

Animals at the age of 3-8 months get sick most often. However, there are reports that during epizootic outbreaks leptospirosis is registered in animals older than two years.

Males get sick more often than females, as they constantly sniff and lick objects that have been exposed to urine.

The source of the infectious agent is sick animals and leptospira carriers, which lasts up to 700 days in dogs, up to days in foxes, and in rodents it can be lifelong.

The causative agent is excreted into the external environment with urine, milk, semen, exudates from the genital tract and feces. Transmission factors are infected feed and water sources, litter and inventory.

The reservoir of the pathogen is murine rodents and wild animals, the infection rate of which is 30–60%. Infection occurs through the digestive tract when feeding raw meat products from sick animals, when eating the corpses of leptospira-carrying rodents. Infected water, especially swampy, slow-flowing reservoirs, poses a great danger of spreading the pathogen. In this case, leptospira can enter the body not only through the alimentary route, but also through damaged areas of the skin (scratches, bites, wounds), eyes, and respiratory tract. The possibility of infection through visible mucous membranes and in utero has been proven.

In most cases, leptospirosis occurs sporadically, and epizootic outbreaks are less common. Most often, leptospirosis is established from May to November and, if it is impossible to break the epizootic chain, conditions for the stationarity of the disease are created. The morbidity and lethality of animals is 40–90%.

Pathogenesis. The pathogenic effect of leptospira is the hemolysis of erythrocytes, which causes anemia, the accumulation of hemoglobin in the blood and the formation of the pigment bilirubin, which stains tissues yellow.

Leptospira, once in the kidneys, violate their filtering ability, as a result of which hemoglobin appears in the urine. The blood coagulation systems are activated. Capillaries are clogged with bloody clots, which leads to necrosis of large areas of tissues and organs.

Symptoms and course. The incubation period lasts 2 days. The course of the disease is acute, subacute and rarely chronic. The disease occurs in two clinical forms - hemorrhagic and icteric.

For the hemorrhagic form, an increase in body temperature up to 40.5-41 0С, depression, loss of appetite, dry cracked nose, severe thirst, fetid breath, bloody diarrhea or constipation are typical.

Sometimes blood appears in the urine. Almost always, muscle pain in the limbs, pain in the abdomen, vomiting with blood, bleeding from the gums and nasal cavity are recorded. As the disease progresses, intense and dramatic emaciation occurs. The skin becomes dry, the eyes sink deeply, the body temperature further decreases to 36–36.5 0C. Urine is excreted in small portions and contains a yellow pigment and protein. Clonic convulsions appear, with the appearance of which the animals can die within a few hours. If the animals survive, they retain paresis, chronic nephritis, and digestive pathology.

The icteric form caused by L.icterohaemorrhagia occurs mainly in puppies and young dogs. At the beginning of the disease, the temperature rises to 40 0C, constipation is recorded, later the feces soften and become covered with blood. Icteric coloration of the mucous membranes of the eyes, oral cavity, and individual areas of the skin appears 2–3 days after the onset of the disease. With the appearance of jaundice, the temperature of the animal drops to 36 0C. Urine is dark yellow with a lot of protein. Often there is itching and conjunctivitis.

pathological changes. An autopsy of dead animals reveals icterus and congestive hyperemia of the liver, kidneys, sometimes with foci of necrosis and hemorrhages in them, as well as in the stomach, muscles and lungs.

Diagnosis. When making a diagnosis, clinical signs, epidemiological data and pathological changes are taken into account with mandatory laboratory tests.

Leptospirosis is differentiated from plague, parvovirus enteritis, infectious hepatitis, salmonellosis, pasteurellosis, listeriosis and alimentary intoxications.

Treatment. In the treatment of animals with leptospirosis, hyperimmune serum, antibiotics (streptomycin, kanamycin, etc.), vitamins (B4, B1, B6 and C), immunomodulators and drugs that stimulate cardiac activity are used.

Prevention and control measures. As a preventive measure, a planned inspection of the breeding stock should be carried out;

examination of blood serum in RMA of imported animals;

culling of infected animals. It is strictly forbidden to feed raw meat and other products obtained from sick animals and leptospira carriers.

In the case of a diagnosis, a restriction is introduced. Sick and suspicious animals are isolated and treated. Forced disinfection is carried out using a 2% hot solution of sodium hydroxide;

2% formaldehyde solution;

clarified bleach solution containing 3% active chlorine;

3% hot solution of sulfur-carbolic mixture.

Manure is disinfected biothermally. Carry out decontamination. Prevent stray animals from entering the farm. Service personnel caring for sick animals or coming into contact with the corpses of dead animals must strictly observe the rules of personal hygiene.

In order to create active immunity, the following are used: polyvalent VGNKI vaccine against leptospirosis, which is intended for immunization of dogs and fur animals;

vaccine against canine distemper, infectious hepatitis, adenovirus, parvovirus enteritis and canine leptospirosis (hexacanivak);

vaccine against canine leptospirosis. It should be noted that the sera and vaccines used do not free animals from leptospirosis.

Restrictions are removed in the absence of cases of disease and death of animals from leptospirosis, the implementation of all veterinary and sanitary measures, final disinfection and the absence of leptospira carriers on the farm.

Botulism (botulismus) is an acute food toxic infection of animals and humans, manifested in the form of paralysis of the pharynx, tongue, lower jaw, a sharp weakening of the tone of the skeletal muscles and a disorder of the gastrointestinal tract.

Etiology. The causative agent of the disease is the spore-forming anaerobic microbe Clostridium botulinum. Of the seven available pathogen types, types A and C are the most virulent. The spores are located subterminally and give the microbe the appearance of a tennis racket. The causative agent of capsules does not form, gram-positive, mobile, 2.5-10 x 0.3-0.8 microns in size.

Spores are highly resistant in the external environment.

Epizootology. Most often, minks, ferrets suffer from botulism, less often arctic foxes, foxes, dogs and cats, regardless of age.

The natural habitat of the causative agent of botulism is the gastrointestinal tract of cattle and some species of carnivores, from where it enters the external environment with feces, where spores continue to retain their biological properties for a long time.

The factors of transmission of the pathogen are infected poor-quality feed, especially dangerous is the meat of dead animals, the carcasses of which have lain uncut for several hours;

corpses of small rodents where toxins have accumulated;

infected meat and fish products.

Infection occurs when eating infected feed in its raw form. Botulism can occur at any time of the year. Enzootic lasts from to 5 days. Mortality can be 70-95%.

Pathogenesis. Botulinum toxin, which enters the body of animals along with food, is absorbed through the mucous membrane of the gastrointestinal tract and penetrates in large quantities into the blood, lungs, liver, and heart.

The toxin circulating in the blood causes vascular disorders leading to the development of hemorrhages, congestion and thrombosis in the capillaries. It disrupts neuromuscular connections, causing muscle relaxation, a drop in muscle tone, paralysis of the heart muscle, asphyxia, and death of the animal.

Symptoms and course. The incubation period lasts from 8–24 hours, rarely up to 2–3 days. The disease, as a rule, proceeds superacutely, less often acutely, which is determined by the amount of toxin that has entered the body.

Sick dogs refuse food, lethargic, experience increased thirst, body temperature is normal. The act of defecation is accelerated, the feces are semi-liquid, fetid, sometimes contain pieces of undigested food, as well as bloody mucus. The disease develops intensively, frequent vomiting appears. In the future, paralysis of the hind limbs may develop, the neck muscles become relaxed, the animals move with difficulty, and a staggering gait is noted. By the end of the disease, the pulse and respiration become more frequent, urination and defecation slow down, peristalsis becomes weakened.

Botulism in arctic foxes and foxes is manifested by depression, impaired coordination of movement, paralysis of the hind limbs, abdominal breathing, and sometimes vomiting.

The minks lose their mobility, the muscles of the body are relaxed, a sharp expansion of the palpebral fissure and pupil is noted, the eyeball protrudes from the orbit of the eye, and there is strong salivation. In the future, due to the onset of a paresis of the hind or forelimbs, the animals cannot rise to their feet, crawl on their stomachs (Fig. 5.). The sick mink lies sprawled.

Rice. 5. Paralysis of the hind limbs in a mink.

If you take it in your hand, in view of the loss of muscle tone, it hangs in your hand like a stocking, does not respond to irritation and sometimes emits a weak squeak.

Shortness of breath is often found. Some minks have diarrhea and vomiting.

The duration of the disease is from several hours to several days.

pathological changes. When the dead minks are opened, catarrhal gastroenteritis, congestive hyperemia of the liver and kidneys, empty intestines and hemorrhages on the pulmonary pleura are revealed.

Diagnosis. The diagnosis is established on the basis of epizootological data, clinical signs and pathological changes, with mandatory laboratory tests. The diagnosis is considered established upon isolation of the causative agent of the disease with characteristic morphological and biological properties, as well as upon detection of botulinum toxin in the pathological material.

When conducting diagnostics, it is necessary to exclude plague, parvovirus enteritis, Aujeszky's disease, poisoning with pesticides, heat or sunstroke.

Treatment. It is not possible to provide medical assistance in view of the hyperacute and acute course of the disease.

Prevention and control measures. When botulism occurs, suspicious meat and fish feed is excluded from the diet of animals or they are fed after thorough heat treatment. Similarly, they do with vegetable feeds that have undergone self-heating and mold.

Particular attention should be paid to the quality of feed after puppies are weaned and in the first days after vaccination. In order to create an active immune system, the following are used: vaccine against mink botulism (alum precipitate toxoid vaccine);

associated vaccine against viral enteritis and mink botulism;

associated vaccine against viral enteritis, botulism and mink pseudomonosis;

vaccine against viral enteritis, botulism, pseudomonosis and canine distemper;

vaccine against viral enteritis and mink botulism.

The sick are isolated and treated. The corpses are destroyed with skins. According to the regulations, forced disinfection is carried out using solutions recommended for spore infections.

The fur farm is considered safe after the elimination of the disease and the final disinfection.

Tuberculosis is a chronic infectious disease characterized by the formation of tubercle nodules in the lungs and other organs and tissues, prone to cheesy degeneration.

Etiology. The causative agent of the disease are microbes belonging to the genus Mycobacterium. Mycobacterium tuberculosis of the human and bovine types cause disease in dogs, cats, and fur animals. In rabbits and minks, tuberculosis is most often caused by mycobacteria of the bovine and avian species.

In terms of morphology and cultural properties, mycobacteria of different species almost do not differ and are thin, straight or slightly curved, immobile rods 0.8–5.5 x 0.2–0.5 µm in size, characterized by high acid and alcohol resistance. Spores and capsules do not form, strict aerobes are cultivated on special nutrient media (Petranani, Gelberg, etc.). In the soil they remain stable for up to 5 years, in manure and bedding - up to 1.5 years.

epidemiological data. Under natural conditions, silver-black foxes, minks, arctic foxes, nutrias, dogs and cats are susceptible to tuberculosis. Nutrias and minks are especially sensitive, among which young animals are more often affected. Tuberculosis was not registered in sables. In rabbits, the disease is recorded mainly in the form of isolated cases in the presence of trouble for tuberculosis of cattle and birds.

The source of the infectious agent is people with tuberculosis, animals and birds from whose body the pathogen is excreted with discharge from the nose, pulmonary sputum, milk, feces and urine.

Transmission factors of the pathogen can be non-decontaminated by-products of animals and birds with tuberculosis;

infected milk, feed, water, bedding, manure, inventory, etc.

In carnivores, nutria and rabbits, the main route of infection is alimentary. Airborne transmission of the pathogen is not ruled out. Puppies can become infected during the suckling period from a sick mother.

In sick minks, intrauterine infection of puppies is noted. By contact, animals can become infected only during the rut (mating).

There is no strict seasonality, however, tuberculosis can be registered in the same farms.

Pathogenesis. The causative agent of tuberculosis, once in the body, penetrates the lungs or other organs, where an inflammatory process develops, manifested by cell proliferation and exudation with the formation of specific nodules-tubercles. With a long course of the disease, large tuberculous foci and cavities can form in the lungs, tuberculous pleurisy develops (especially in dogs and cats). From the lungs, mycobacteria often enter the bloodstream, which leads to a generalization of the process and the development of tuberculosis foci in various organs and tissues.

Symptoms and course. The duration of the incubation period has not been reliably established, however, with experimental infection with the causative agent of tuberculosis, an allergic reaction develops on days 15-17.

In young minks (puppies 15-20 days old), tuberculosis proceeds malignantly, often in the form of a generalized lesion of internal organs.

In adult minks, signs of the disease appear as deep and extensive lesions in the internal organs. Less commonly, there is cough, nasal discharge, abscesses in the head and neck, diarrhea, severe exhaustion.

In foxes, arctic foxes and nutrias, tuberculosis is less malignant.

So, in the pathology of the intestinal tract, vomiting, diarrhea, and severe emaciation are observed (Fig. 6.).

Rice. 6. A fox with tuberculosis.

With the defeat of the respiratory tract, cough, wheezing, shortness of breath, shortness of breath are noted. If the liver is involved in the process - jaundice of the mucous membranes;

nervous system - excitation, loss of vision, paresis and paralysis of the limbs.

In 5-7-month-old fox puppies, one or both eyes are very often affected. At the same time, the eyeball is enlarged in volume, protrudes from the orbit, and corneal clouding is observed. After 15–30 days, the eyeball opens and a brown liquid flows out of it.

In rabbits, two forms of the disease are distinguished: pulmonary (cough, rapid breathing, shortness of breath) and intestinal (loss of appetite, diarrhea and emaciation).

Dogs show signs of lung (shortness of breath, short, dry cough, and nasal discharge) and gastrointestinal (vomiting, down the nose) signs.

In cats, a sharp emaciation, anemia, shortness of breath, suppuration of the parotid, submandibular and prescapular lymph nodes are recorded.

Often the skin and underlying tissues on the head, neck, eyelids, bridge of the nose and cheeks are affected in the form of fluctuating tumors containing a yellow, crumbly mass.

pathological changes.

in minks: - miliary and nodular tubercles in the lungs and under the pleura (when they are cut, a thick curdled mass or purulent content is found);

- focal or diffuse tuberculous tuberculous lymphadenitis of the mediastinal, mesenteric and bronchial nodes with the presence of cheesy or purulent foci;

- a sharp increase in the spleen (8-10 times) with the presence of tubercles;

- tuberculous tuberculosis of the serous integument of the peritoneum;

- the presence of specific tubercles in the liver, udder, ovaries, uterine wall, kidneys and on the serous integument of the intestine;

- exhaustion;

in foxes and arctic foxes:

- miliary, nodular or nodular tubercles in the lungs;

- tuberculous lymphadenitis of the mediastinal and mesenteric nodes;

- the presence of small tubercles in the kidneys;

- tuberculous testiculitis (in male foxes);

- wasting, anemia and sometimes jaundice;

in nutria:

- miliary or macrofocal tuberculosis in the lungs;

- the presence of small tubercles on the mucous membrane of the small intestines, as well as in the liver and kidneys with their ulceration;

- tuberculous tuberculosis of the mesenteric lymph nodes;

- in some cases, an increase in the spleen with the presence of tubercles.

When making a diagnosis, clinical diagnosis is taken into account.

epizootological data, results of autopsy, allergic and bacteriological studies.

Tuberculinization is carried out using purified (PPD) tuberculin for mammals, which is administered:

- to dogs and fur-bearing animals (except for minks) in the area of ​​the inner surface of the thigh, intradermally at a dose of 0.2 ml;

- to cats in the region of the inner surface of the ear, intradermally at a dose of 0.2 ml;

- to minks (foxes and arctic foxes, V.P. Shishkov, V.P. Urban, 1991) intrapalpebrally, in the middle part of the upper eyelid, at a dose of 0.1 ml (for foxes and arctic foxes - at a dose of 0.2 ml).

– in rabbits and nutria, allergic diagnostics have not found application.

Accounting and assessment of the reaction to tuberculin is carried out in dogs, cats and fur animals after 48 hours and animals are recognized as reacting when swelling is formed at the site of tuberculin injection.

Bacteriological examination is of decisive importance in the diagnosis of tuberculosis. To do this, whole carcasses of small animals are sent to the laboratory, and from adult animals - affected lymph nodes, pieces of parenchymal organs and tissues.

The diagnosis is considered established by isolating the culture of the causative agent of tuberculosis or by obtaining a positive bioassay result.

Differential diagnosis. Tuberculosis must be differentiated from actinomycosis and pseudotuberculosis.

Treatment. Sick rabbits, cats and dogs are killed. For therapeutic purposes, until the fur matures, sick fur animals are fed with tubazid or isoniazid at the rate of 20 mg/kg of body weight, after which the animals are killed. The remaining animals of the disadvantaged group are fed with tubazid in a prophylactic dose. At the same time, it is recommended to add vitamin B6 (pyridoxine) at a dose of 1 mg and ascorbic acid at a dose of 30 mg per animal per day to the feed.

Immunity in tuberculosis is non-sterile. In order to prevent tuberculosis, mink puppies at the age of 20-30 days are immunized with the BCG vaccine, which is administered at a dose of 0.2 mg subcutaneously, into the region of the inner surface of the thigh.

Prevention and control measures. When a diagnosis is established, quarantine is imposed. In dog breeding kennels, females with offspring are killed, the skins from them are used without restriction. Animals of the unfavorable group are allergic tested every 60 days until single group negative results are obtained and quarantine is lifted after the final veterinary and sanitary measures.

In all other categories of fur farms, quarantine is removed after the slaughter of sick animals, in the absence of changes typical for tuberculosis in organs and tissues in fallen and killed animals during one production cycle (from weaning to slaughter for skins) and the final veterinary and sanitary events.

Quarantine from a dysfunctional rabbit farm is removed 1 year after the last case of the disease and the final veterinary and sanitary measures. For disinfection, the drug DP-2, a 1% solution of glutaraldehyde, an alkaline solution of formaldehyde (containing 3% formaldehyde and 3% sodium hydroxide) are used.

Chlamydia (chlamydiosis) is a contagious disease of many animal species, characterized by the development of pneumonia, keratoconjunctivitis, polyarthritis, encephalitis, and urogenital pathology. Zooanthroponosis.

Etiology. The causative agent of the disease are bacteria of the species Chlamydia psittaci, Ch. pneumoniae, Ch. trachomatis, which are small intracellular bacteria characterized by a unique development cycle with the formation of cytoplasmic inclusions. Chlamydia are predominantly round in shape with a diameter of 0.2-0.5 microns, multiply by binary fission, contain RNA and DNA, are cultivated on chicken embryos, do not form spores and capsules, are immobile.

Epizootology. Chlamydia infection is widespread among foxes, arctic foxes, dogs and cats. In addition, chlamydia affects a large number of species of farm animals and over 70 species of birds, as well as a significant number of wild animals, fish, amphibians, and insects that create a natural reservoir of infection, which contributes to the emergence of secondary foci of chlamydia. They are also isolated from hares and muskrats. The possibility of interspecific transmission of the pathogen has been established.

Chlamydia most commonly affects animals between the ages of 5 weeks and 9 months.

The source of the infectious agent is sick animals and bacteria carriers, as well as animals with a latent form of the disease, which excrete the pathogen into the external environment with discharge from the eyes and nasal cavities, as well as when sneezing and snorting, with urine and feces, with saliva and exudate genital tract.

The transmission factors of the pathogen are infected food, water, care items, wool, overalls.

Infection occurs by respiratory and alimentary routes, as well as by direct contact, through damaged areas of the skin, intrauterine and sexually.

The disease manifests itself in the form of sporadic cases and endemic outbreaks. There is no strict seasonality, but stationarity of the infection has been established.

Pathogenesis. Having penetrated into the body, the pathogen multiplies in the epithelial cells of the mucous membranes and macrophages. Then it penetrates into the blood and enters the internal organs, lymph nodes, joints, and even the brain and spinal cord, where it causes inflammatory and degenerative processes.

Symptoms and course. The incubation period is 5-10 days. The disease proceeds acutely (80%) and chronically (20%).

In the acute course of the disease, serous develops, and then catarrhal purulent conjunctivitis (85.4%) and rhinitis (88.4%).

At the onset of the disease, mild fever is noted, lasting several days. Moreover, animals retain their appetite. Conjunctivitis lasts from several days to several months, and sometimes takes a chronic course. Initially one is affected, and then both eyes.

Pneumonia and diarrhea are subclinical. Quite often, abortions and peritonitis are recorded.

pathological changes. At autopsy, the following are found:

- catarrhal bronchopneumonia;

- serous-purulent conjunctivitis, rhinitis;

- serofibrinous pericarditis;

- granular dystrophy of the liver, kidneys and myocardium;

- hyperplasia of the spleen.

Diagnosis. The diagnosis is made in a complex manner, taking into account epizootological data, clinical signs, the results of an autopsy and laboratory tests.

The result of the research is considered positive in the isolation and identification of chlamydia from the pathological material. In addition, immunological methods have been proposed for the diagnosis of chlamydia: RSK, RIF, ELISA and PCR.

When making a diagnosis, it is necessary to exclude plague, pasteurellosis, mycoplasmosis, herpes virus infection (in cats), infectious rhinitis and keratoconjunctivitis, listeriosis, where laboratory tests are of paramount importance.

Treatment. When providing therapeutic assistance, it should be taken into account that chlamydia are resistant to sulfonamides, neomycin, biomycin, penicillin and streptomycin. There are no specific treatments.

The most effective are tetracycline drugs (oxytetracycline, tetracycline hydrochloride, doxycycline, chlortetracycline), but dairy products containing calcium and magnesium ions, which form insoluble complexes with tetracycline drugs (except doxycycline) should be excluded from the diet.

Prevention and control measures. These measures include strict adherence to veterinary and sanitary and zoohygienic rules, the principles of "empty-busy", microclimate, and the timing of disinfection.

A clinical examination is carried out daily, according to the results of which, taking into account serological studies, sick animals are isolated and treated.

Manure is disinfected biothermally, corpses are destroyed, forced disinfection is carried out using a 3% hot solution of sodium hydroxide, 2% formalin solution, clarified bleach solution (containing 3% active chlorine), 5% soda ash solution .

In order to create active immunity, a vaccine against panleukopenia, rhinotracheitis, calicivirus infection and chlamydia in cats (inactivated) - Multifel-4 - was proposed.

An economy is considered safe if there are no sick animals in it;

with negative results of serological studies of the entire livestock and after the final veterinary and sanitary measures.

Dermatophytosis of carnivorous and fur-bearing animals is a fungal disease caused by pathogenic fungi of the genus Microsporum and Trichophyton.

Microsporia (microsporosis) is a highly contagious disease characterized by inflammation of the skin, the appearance of sharply limited rounded spots on it, breaking off the hair on the affected areas, followed by their loss. Man also suffers from microsporia.

Etiology. The causative agent of the disease in dogs, cats, rabbits and fur animals is Microsporum canis, M. lanosum, M. felineum;

in cats and dogs, M. gypseum (M. lanosum bodiu).

In the pathological material obtained from the affected area, a branched septate mycelium and rounded unicellular spores 2–3 μm in diameter are found, located mosaically in the form of a sheath at the base of the hair on its outer side (Fig. 7.). The pathogen is cultivated on special nutrient media (Sabouraud agar, Czapek agar, wort agar) at a temperature of 20–30 0C.

Fig.7. Microsporum canis.

Pathogen spores, with the help of which the pathogen is reproduced, retain their biological activity in the affected hair for 2–5 years, in wool for 2–7 years, in manure for 8 months, and in soil for 2 months.

Epizootology. Cats, fur-bearing animals, rabbits, dogs are ill with microsporia. Young animals are more sensitive to it. It has been established that in 85% of cases people become infected with microsporia from cats.

The source of the infectious agent is sick animals and carriers, which excrete the pathogen with falling hair, scales and crusts. Homeless cats and dogs, as well as rodents (pathogen reservoir) are of particular danger in maintaining epizootic ill-being. The carrier of the pathogen can be blood-sucking insects.

The pathogen transmission factors are infected care items, common muzzles, infected feed, bedding, overalls, cages and houses in which sick animals were kept.

Infection occurs directly upon contact of sick animals with healthy ones, as well as after feeding by-products (heads) from sick animals. Predispose to the disease - high humidity, monotonous nutrition with a deficiency of trace elements and vitamins, the presence of skin damage and scratches on the surface of the body.

The disease is recorded throughout the year with a pronounced rise in incidence in spring and autumn. The disease has a pronounced stationarity and proceeds in the form of enzootic with livestock coverage from 4 to 70%.

Pathogenesis. Spores or mycelium of the fungus, getting on the skin, multiplying, affects the hair follicles, releases exotoxins and proteolytic enzymes, which cause an inflammatory reaction on the skin. It thickens, swells, the mouths of the hair follicles contain purulent exudate, which, drying up on the surface of the skin, forms scales and crusts.

Symptoms and course. The incubation period is 8-30 days.

There are superficial, deep and latent (subclinical) forms of the disease. In the vast majority of cases, microsporia occurs in a latent form, sometimes superficial.

At the first stage of the disease, clinical signs are characterized by the formation of depigmented (gray), hairless spots (mycotic foci), covered with scales, which are localized in the nose, eyes, ears, neck and extremities.

Rice. 8. Microsporia in a mink With a generalized spread of the pathogen, damage to the skin and hair is observed throughout the body of the animal. The spots, as a rule, have a rounded, well-defined shape. In the future, mycotic foci can merge with each other, forming ash-colored crusts. When pressing on the affected areas, a purulent exudate appears from the mouth of the hair follicles, which dries up and forms crusts and scabs. (Fig. 8.) The deep form of microsporia is extremely rare, it is registered in puppies and kittens in the area of ​​​​the eyes, at the base of the ears, on the forehead and paws in the form of spots with small bubbles and gray-yellow crusts.

In nutria, the disease is accompanied by severe itching and can be fatal.

Diagnosis. Animal microsporia is diagnosed on the basis of epidemiological data, clinical examination, mycological examination results and the luminescent method. The affected hair, scales, crusts, as well as deep scrapings (until a drop of blood appears) from the affected, untreated skin areas are sent to the laboratory.

The luminescent method involves the study of the skin of a sick animal or affected hair placed in a Petri dish. The study is carried out in a darkened room using a mercury-quartz lamp PRK-2, PRK-4, LD-130 with a Wood filter. The affected areas luminesce in the form of an emerald green glow. In animals of black color, the glow of affected hair may be absent. It should be taken into account that rivanol, vaseline and salicylic acid give nonspecific fluorescence.

Microsporia must be differentiated from trichophytosis, scab, scabies, avitaminosis A and group B, dermatitis of non-infectious etiology, which is based on laboratory tests and light microscopy.

Treatment and specific prevention. With dermatomycosis, fungistatic drugs are used that can delay the growth of the fungus. For this purpose, the following medicines are recommended for use: 10% salicylic acid solution in 5% iodine solution;

3-5% solution of iodine monochloride;

ointment "YAM";

ointment Vaganova;

trichothecin liniment;

oily 15% solution of dermaftox;

5-10% phthalan ointment;

5% amikazol ointment;

ointment "Mikozolon";

ointment "Mikoseptin";

aerosol "Fungiderm";

aerosol "Zoomikol", etc. Along with local treatment, one should use agents that affect the body as a whole: vitamin therapy, fungiostatic antibiotics (griseofulvin, nizoral, etc.), as well as antihistamines: pipolfen, suprastin, tavegil, fen carol, dexamethasone. In the course of treatment, it should be remembered that dogs are hypersensitive to turpentine, and cats to tar, creolin and lysol.

As specific means of treatment, vaccines are used that have a therapeutic and prophylactic effect: the inactivated vaccine against dermatophytosis "Polivak-TM" includes 8 species of fungi from the genus Trichophyton and Microsporum;

inactivated vaccine against dermatophytosis "Wakderm";

inactivated associated vaccine against dermatophytosis in carnivores, coypu and rabbits.

Prevention and control measures. All nascent young animals that have reached vaccination age are subject to immunization.

The farm (farm) where an animal disease is detected is recognized as unfavorable and restrictions are introduced. Those who are sick or suspected of being sick are isolated and treated. Crusts, wool, scales - destroy. All animals are subjected to a clinical examination every 10 days and, if sick animals are detected, disinfection is carried out using a hot 2% formaldehyde alkaline solution.

Manure and bedding are disinfected. Overalls twice a week are heeled and carefully ironed. Persons caring for sick animals must observe the rules of personal hygiene.

The skins of sick animals are disinfected. Carry out deratization and prevent stray dogs and cats from entering the farm.

Restrictions are removed 2 months after the last case of detection of sick animals and the final disinfection with subsequent whitewashing with a 20% suspension of freshly slaked lime.

Trichophytia (trichophytia) (trichophytosis, ringworm) is a contagious fungal disease characterized by the formation of rounded, sharply limited spots on the skin with hair broken off at the base or exudative dermatitis and purulent folliculitis, with a thick bran-like crust on the surface of the affected area.

Etiology. The causative agent of the disease is imperfect mold fungi, in the vast majority of cases belonging to the genus Trichophiton mentagrophytes (gypseum) and less often Tr.verrucosum. Cultivated on special nutrient media Saburo, Litman, wort agar. The spore diameter in Tr.

mentographites is 3–5 µm, while in Tr. verrucosum, 5–8 µm. The mycelium of the fungus is branching. The pathogen retains its biological properties indoors, on care items for 4-8 years, in the soil - 3-4 months.

Resistant to freezing, drying, exposure to direct sunlight.

Epizootology. Trichophytosis affects foxes, arctic foxes, dogs, nutrias, rabbits and, very rarely, cats. Susceptible animals of all age groups, but most often the disease is recorded in young animals. A person also suffers from trichophytosis.

The source of the causative agent of infection are sick and recovered animals, which excrete the pathogen into the external environment with scales, crusts and hair (wool) from the affected areas of the skin. The reservoir of the pathogen in the external environment are mouse-like rodents, stray cats and dogs with an atypical form of the disease.

The pathogen transmission factors are cages and houses where sick animals were kept in the absence of their sanitation, as well as infected equipment, care items, overalls, bedding.

Infection occurs through direct contact between sick and healthy animals, as well as through infected environmental objects. The spores of the fungus can be airborne. The disease in fur animals can appear after feeding slaughterhouse waste from animals suffering from trichophytosis.

Predisposing factors for infection of animals are various mechanical damage to the skin (scratches, scratches, abrasions, etc.), as well as damp rainy weather.

The disease has a mass distribution, especially during the molting of animals, when fluff and wool are blown around the farm by the wind. Sporadic cases of animal disease are observed throughout the year. Enzootic outbreaks are recorded in the winter-spring period. The resulting disease takes a stationary character.

Pathogenesis. Reproducing in the stratum corneum of the epidermis, rich in keratin, the pathogen loosens it, causing inflammation. The hair loses its luster, becomes brittle and breaks off, exudate sweats onto the surface of the skin, gluing the resulting scales, turning them into crusts.

Symptoms and course. The incubation period lasts from 7 to 28 days. The nature of the course and manifestation of the disease is seriously affected by the conditions of keeping and feeding, the level of natural resistance and the age of the animals.

Depending on the nature of the manifestation of the pathological process, there are superficial, deep (follicular) and atypical (erased) forms of the disease.

In carnivorous animals and rabbits, lesions are localized mainly on the head, neck, and limbs. They can be located singly or be diffusely scattered over the entire surface of the body. At the same time, a deep (follicular) form of trichophytosis is more often recorded, when single foci with exudative inflammation and bursting vesicles form multiple foci of large sizes. Intense exudation of the affected areas is accompanied by the formation of dense, thick crusts, when pressed, purulent exudate is released from the hair follicles. In the future, oval and rounded spots appear, covered with hard-to-remove crusts. In some cases, itching is sharply expressed in these places, and abrasions soaked in blood can form.

In young coypu, the disease proceeds in the form of deep infiltration dermatomycosis with dissemination of the process, which is clinically manifested by the formation of round hairless areas covered with gray-brown crusts on the head, neck, sides, trunk, and less often on the limbs. Itching is absent or mild. The number of foci varies from 5 to 12. They rise above the surface of the skin by 1–1.5 cm. When the crusts are removed, bloody-purulent exudate is released at the sites of the lesion. The healing of the foci begins from the center and slowly moves towards the periphery.

Diagnosis. In the process of establishing the causes of an animal disease, epizootological data, characteristic clinical signs of the disease, and laboratory results are taken into account.

In the process of diagnosis, microsporia, scabies, scab, skin lesions of non-contagious etiology should be excluded.

Treatment. In addition to the means indicated above, warm 3-5% solutions of iodine monochloride or a 0.25% solution in fish oil or vaseline oil - trichothecin are used to treat the affected areas.

When introduced into the diet at the same time 0.3 g of ground sulfur and 6 g of BVK per day per head, a good therapeutic and prophylactic effect is recorded. In addition, biological preparations are widely used for treatment, in particular, the Mentavak vaccine.

Prevention and control measures. The general system of preventive measures consists in strict observance of veterinary and sanitary rules;

optimal conditions for keeping and feeding;

implementation of sanitation of rooms, sheds and cages.

When a disease occurs, the economy is declared unfavorable and restrictions are introduced, which are carried out similarly with microsporia.

FUR VIROSES Canine distemper (febris catarrhalis infectiosa) (infectious catarrhal fever) is an acute viral disease characterized by fever, catarrh of the mucous membranes, pneumonia, skin exanthema, and damage to the nervous system.