As a result of diseases of the skin of fur-bearing animals, the value of the fur skin decreases, and sometimes the value is completely depreciated (more about). That is why the study of these diseases and methods of combating them is so important. And today we invite you to talk about diseases of the fur of wild fur-bearing animals.

Pruritic scabies

The causative agent of scabies

The specific mite of fox scabies has a rounded body, dirty white, light brown in some places. It often infects foxes and arctic foxes on fur farms. The size of the female tick is 0.42 by 0.31 millimeters, the male is 0.24 by 0.18 millimeters. On the ventral side you can see 4 pairs of legs, at the tips of which there are either suckers or long bristles. The jaws of the tick are of the gnawing type.

In nature, foxes become infected with equine mange pathogens. The body of this tick reaches a length of 0.2-0.5 millimeters. On the back there are scaly outgrowths and bristles, which point backwards with their points. The proboscis has a horseshoe shape. The legs are short and thick.

Such mites spend their entire lives, at all stages of development, on the body of their owner. They live in the thickness of the skin and feed on lymph, making winding passages in the epidermis. The female can lay from 20 to 50 eggs at a time, from which larvae will appear in 3-7 days, which will turn into nymphs after a few days. After 2-3 molts, the nymphs become sexually mature ticks. It takes 15-20 days for the full development cycle of the itch mite.

Sources of infection

The source of infection, of course, is sick animals. Infection occurs through direct contact with them or through care items, cages in which sick animals were kept. Under natural conditions, infection can also occur when foxes and wolves eat the corpses of horses that were affected by scabies.

How does itchy scabies occur?

Initially, in foxes and arctic foxes that are sick with scabies, the paws, area inner surface hips, tail root and head. In the future, the process can spread to the entire surface of the body. On the affected areas you can find small nodules that turn into blisters. As a result of scratching, a secretion is released from the affected areas, which, when dried, forms crusts. The fur begins to fall out, and falls off in places where there is thick hair. At the same time, the animal itself loses its appetite, looks sick and may die.

To eliminate the epizootic, it is advisable to destroy sick foxes. Their burrows must be treated with a sharp-smelling acaricidal agent and then buried. Despite the fact that this process is labor-intensive, it is necessary to prevent the spread of scabies.

Treatment of pruritic scabies

Treatment of dogs and caged fur-bearing animals that have become ill with pruritic scabies should be carried out with mite-killing agents, with disinfection of the room where they are kept. However, first you should remove dirt and crusts from the surface of the sick animal’s body, and wash it with warm water. The treatment is long-term. And objects with which the animal came into contact before and during the disease are recommended to be disinfected.

Ironwort or demodicosis

This is the name for scabies, which is caused by mites from the Demodex family. Among fur-bearing animals, foxes and arctic foxes most often suffer from demodicosis.

The causative agent is a tick, has a worm-like shape and very short legs with 2 claws at the ends. The length of the tick can be 0.25-0.3 millimeters.

How does ironworm infection occur?

Infection occurs through contact of a sick animal with a healthy one. At the same time, the presence of defects on the skin due to previous infections increases the risk of infection. skin diseases. For example, the animal already had scabies or eczema. Whereas animals having healthy skin, rarely get sick.

The gland in fur-bearing animals can occur either in a scaly or pustular form. Moreover, the scaly form usually turns into pustular. The latter is more malignant and more difficult to treat. Fur completely falls out on the affected areas, folds form on the skin, and lymph begins to ooze from the pustules, which forms crusts when it dries. The lesion is complicated by secondary infection. Due to severe intoxication, the animals die.

In order to determine the presence of this type of mite, a deep scraping of the skin is taken from the affected areas, or even better, from the contents of the pustules.

Treatment of the iron worm

By analogy with dogs that can become infected from sick animals, the best remedy is considered to be a treatment intravenous administration 1% trypansinia solution or methylene blue at a dose of 0.01 grams per 1 kilogram of live weight, repeated 2-3 times with a weekly interval. At the same time, it is necessary to rub finely dispersed sulfur into the skin affected by the tick, use 4-carbon chloride, Peruvian balsam, and iodine.

To prevent and eliminate sources of infection, animals suspected of the disease are isolated and treated. And all objects with which they came into contact are disinfected.

Colibacillosis of fur-bearing animals is predominantly an acute infectious disease of young and adult Arctic foxes, foxes, sables, nutria and minks. Colibacillosis in young animals predominantly occurs septically with symptoms of diarrhea, damage to the central nervous system and respiratory organs, in adults - in enteritic or enterotoxemic forms, as well as in the form of abortions (birth of still puppies), cystitis, otitis, mastitis, urocystitis and meningoencephalitis.

Pathogen– enteropathogenic E. coli, including different serogroups of Escherichia coli, differing in enzymatic activity, antigenic and other biological properties. Fur-bearing animals are most often affected by Escherichia serogroups O86, O2, O26, O55, O78, O125, O111, and O20.

Their K-antigenic composition and toxicogenic properties have not been sufficiently studied. Up to 50% of hemolytic strains of Escherichia are isolated from fur-bearing animals.

Epizootological data. The main source of colibacillosis is sick young animals, adult animals - carriers of pathogenic Escherichia, as well as feed, drinking water, bedding and animal care items contaminated by them. The main route of infection is nutritional; intrauterine infection cannot be ruled out. Young Arctic foxes and foxes are most susceptible to colibacillosis in the first 10 days after birth. Mink and sable are more resistant to colibacillosis, whose puppies become ill only during the laying period. Pregnant and lactating animals are sensitive to colibacillosis. The disease is focal in nature and occurs enzootically. Predisposing factors such as inadequate and poor-quality feeding play an important role in the occurrence of colibacillosis, accompanying illnesses, violation by owners of fur-bearing animals of conditions of detention, veterinary, sanitary and zoohygienic rules, as well as climatic conditions and season of the year. In fur farms, colibacillosis most often occurs in the warm season, when the sanitary condition on fur farms is unsatisfactory, and those used for feeding meat products difficult to keep fresh.

Pathogenesis enteritic forms of colibacillosis in animals are almost not described, although it may not differ much from the mechanism of colibacillosis in other animals. In animals, the disease can begin with damage to the skin or mucous membranes, followed by the formation of abscesses and phlegmons. In case of infection of the excretory and secretory organs of animals, vaginitis, metritis, urethritis, mastitis and other lesions occur. The severity of the disease and the incubation period vary significantly and directly depend on the immunological state of the animal’s body, the pathogenicity of the pathogen and the gates of infection. Incubation period for minks, arctic foxes and foxes is 1-5 days. Animal puppies usually die at 1-10 days of age. The course of colibacillosis is usually acute or subacute in enteritic and enterotoxemic forms and chronic in cases of damage to the central nervous system.

Clinical signs. With the enteritic form of colibacillosis, puppies constantly squeak, worry, their hair is tousled, matte in color, and contaminated with feces. Feces are liquid with gas bubbles, yellow-green, brownish or white-yellowish in color, often mixed with mucus. After 1-2 days, sick puppies become lethargic and cold to the touch. If medical care is not provided, animals die within 1-5 days. In older puppies, colibacillosis occurs with the same symptoms, but over a longer period of time. Less commonly observed is the encephalitic form, which affects puppies aged 3-50 days. Sick animals are excited or depressed, their skull enlarges, has an irregular shape, and upon palpation we note non-fusion of the skull bones. In sick animals, coordination of movements is impaired, paresis of the limbs and convulsions occur. With this form of the disease, up to 16% of puppies die in some farms. In adult female foxes and arctic foxes, signs of colibacillosis are weakly expressed and manifest themselves mainly in the form of abortions and the birth of still puppies.

Pathological changes. In the acute course of the disease, when autopsying dead animals, we find signs of catarrhal or hemorrhagic inflammation of the intestines. Mesenteric The lymph nodes edematous, hyperemic and often with hemorrhages. The liver and kidneys are clayey to dark cherry in color with pinpoint hemorrhages, some areas of the lungs are edematous. In the chronic course of colibacillosis, the corpses of dead animals are emaciated, the mucous membrane is cyanotic. The encephalitic form is characterized by deformation of the skull bones, injection of brain vessels with hemorrhages, and possible accumulation of purulent exudate or pinkish fluid in the ventricles of the brain.

Diagnosis. The diagnosis of colibacillosis is made on the basis of epizootic, clinical signs and the results of bacteriological examination of feces from sick animals, and the results of examination of pathological material from dead animals. The leading ones are bacteriological.

Differential diagnosis. Colibacillosis in animals must be differentiated from, klebsiellosis, mycotoxicosis, and.

Immunity and means of specific prevention. In newborn animals, immunity is mainly passive, acquired with colostrum in animals older than 15 days; active immunity is possible when using a polyvalent vaccine against salmonellosis and colibacteriosis of fur-bearing animals, polyvalent serum against colibacillosis (escherichiosis) of farm animals.

To vaccinate animals, a polyvalent vaccine against salmonellosis and colibacillosis of fur-bearing animals is used. The vaccine is used in farms that are unfavorable and threatened by salmonellosis or colibacillosis. Immunization is carried out only to clinically healthy animals of the main herd and puppies. It is prohibited to vaccinate females in the second half of pregnancy. The vaccine is administered subcutaneously into the area of ​​the inner thigh, 2-3 hours before feeding.

Adult livestock of foxes and arctic foxes are vaccinated 2-3 weeks before the rut or in the first half of pregnancy, 2 times with an interval of 8-10 days, in doses of 3 ml for foxes - the first injection and 5 ml for the second, for arctic foxes 2 and 3 ml, respectively.

Before vaccination, young foxes and arctic foxes are examined and divided into two groups:

1st. Clinically healthy animals.

2nd. Animals are weak, developmentally delayed, sick.

Young animals of the first group are vaccinated from 30-45 days of age; fox puppies - 2 times in doses of 1 and 2 ml; Arctic fox puppies - 3 times in doses of 0.25, 1 and 1.5 per month, with an interval of 8-10 days.

Puppies of the second group are treated and, after recovery, vaccinated as indicated above. Adult nutrias and their puppies, in the event of salmonellosis or colibacillosis occurring on the farm (on the farm), are vaccinated in doses and terms as for arctic foxes.

Immunity in animals occurs 10-12 days after the last injection of the vaccine and lasts up to 6 months. Deworming of fur-bearing animals is not allowed for 7 days before vaccination and 14 days after it.

Prevention and control measures. Carry out general zoo-hygienic and veterinary-sanitary measures. The animals are provided with complete and high-quality food, disinfection, deratization and disinfestation are carried out in a timely manner, and females that have given birth to dead puppies or aborted are culled from the herd.

Sick animals must be isolated in separate cages, and those released must be disinfected. Isolated animals are kept on a starvation diet for 12 hours, and then given highly nutritious and easily digestible food (chopped root vegetables, grass, feed pellets), as well as dairy products containing acidophilus bacteria, adding chloramphenicol or biomycin to them for 3-4 days in a row, 25 -30 mg/kg live weight every 8-12 hours, furozolidone or furagin 30 mg/kg live weight, syntomycin 0.2 mg/kg live weight.

For therapeutic purposes, streptomycin, propomycelin, colimycin are effective, and for prophylactic purposes, propomycelin and PABA are effective. They are used in a mixture with food monthly from February until the end of whelping: 3-5 days propomycelin, 5-8 days PABA.

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CONTAGIOUS DISEASES

FUR ANIMALS

(MONOGRAPH)

VITEBSK, 2008

veterinary sciences, professor

scientist of the Republic of Belarus;

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

tological anatomy and histology of the UO VSAVM;

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

Zitology and Invasive Diseases UO VSAVM;

Nikolaenko M.F. – Assistant at the Department of Diseases of Small Animals and Birds, VSAVM.

Reviewers: Medvedev A.P. – Doctor of Veterinary Sciences, Professor of the Department of Microbiology and Virology of the VSAVM;

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

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

Contagious diseases of fur-bearing animals Monograph / A.I. Yatusevich, V.S.

Prudnikov, N.F. Karasev, M.F. Nikolaenko. - Vitebsk: OU 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 (protocol No. of 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. BBC: 48. © A.I. Yatusevich et al., © Vitebsk Order of the Badge of Honor

State Academy of Veterinary Medicine", CONTENTS Page.

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

Due to a number of features, infectious diseases represent the most dangerous group of diseases that exist in nature as a result of the continuity of the epizootic process and can, under certain conditions, cause great economic damage to fur farming, and some of them pose a danger to humans.

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

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

BACTERIOSIS OF FUR ANIMALS Escherichiosis is an infectious disease accompanied by profuse diarrhea, signs of severe intoxication and dehydration of the body.

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

The pathogen in feces and secreted exudate retains its biological activity for up to 30 days, in soil and water for up to several months.

Epizootology. Young newborns are susceptible to the disease at the age of 1–4 days, and 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 who intensively excrete the pathogen in feces and sometimes in urine.

Factors of transmission of the pathogen include infected food, water, equipment, bedding, special clothing, etc. Carriers are wild rodents and birds.

Infection occurs both during childbirth, in particular, when hygiene rules are not followed, and when the conditions of feeding and keeping animals are violated. The pathogen enters the body through food, water, and less commonly through aerogenic routes.

The disease occurs in the form of enzootics, covering a significant number of animals, without strictly defined seasonality. In permanently unfavorable farms, the mortality rate of puppies can reach 15–25%.

Pathogenesis. Enteropathogenic strains of the pathogen, once in the gastrointestinal tract, cause the development of dysbiosis and intoxication. Subsequently, penetrating into the bloodstream, they cause a state of septicemia.

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

With the enteritis form, a decrease in appetite is noted, the puppies become inactive, restless, and squeak. Signs of inflammation of the gastrointestinal tract develop intestinal tract– feces become liquid, mushy, and yellow in color. Subsequently, the diarrhea intensifies, the color of the excrement becomes gray-white or dark gray with an admixture of mucus, a fetid odor, and sometimes the feces foam. In suckling puppies, the excrement contains clots of coagulated milk, sometimes mixed with blood. In severe cases, the act of defecation becomes more frequent and becomes involuntary. The fur near the anus, on the tail, and hind legs is wet and contaminated with dried, sticky feces. Body temperature at the onset of the disease reaches 40.0–41.5 °C, and during the agonal period it drops to normal and even lower. Puppies lose weight rapidly, their fur loses its shine, becomes disheveled, and coordination of movement is impaired due to weakness of the hind limbs (Fig. 1). In acute cases, the disease ends in death within 3–6 days. For substroma - on days 10–16.

Rice. 1. Mink puppy with enteritic 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. Arctic fox puppy with escherichiosis.

Dropsy of the brain. Comatose state.

In infected pregnant females, abortions or stillbirth of puppies, decreased appetite and depressed state are recorded.

Puppies have the most nutria early sign The disease is anxiety, expressed in continuous squeaking. The hair and skin near the anus are contaminated with feces. At light massage In the abdomen, liquid feces of heterogeneous consistency, yellow-green or white-yellow in color with bubbles of gas and mucus, are released from the anus.

Pathological changes. When autopsying corpses that died from escherichiosis, the following is revealed:

– enlarged spleen (splenitis);

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

– serous lymphadenitis of the mesenteric nodes;

– exicosis.

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

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

In addition, the diagnosis will be recognized as established when Escherichia, pathogenic for white mice, is isolated from at least two organs.

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

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

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.

Disinfect enclosures, sheds, houses, equipment 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.

Immunization of females is carried out in order to create passive immunity in puppies, using a polyvalent vaccine against salmonella and escherichiosis of fur-bearing animals. Create an optimal technological regime for keeping animals. Deratization is carried out. The corpses of dead animals are destroyed. Manure is disinfected biothermally.

Restrictions are lifted if there are no sick animals, healthy offspring are obtained and veterinary, sanitary and special measures are implemented in full.

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

Etiology. The causative agent of the disease is a gram-negative, motile rod with rounded ends, does not form spores or capsules, and is relatively resistant to external environment. The disease in small animals is most 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, which excrete the pathogen in feces, urine, discharge from the nasal cavities, saliva and milk. Factors of transmission of the pathogen are infected feed (meat and bone and fish meal, slaughterhouse waste), in addition, water, bedding, and care items. The pathogen can be carried by mice, rats, birds, and insects.

Infection occurs through the nutritional route. Aerogenic and intrauterine infection is possible. Outbreaks of the disease are recorded at any time of the year, if there is a susceptible population of animals. The disease is characterized by stationarity, with intensive development of the epizootic with a wide coverage of a large number of animals.

Pathogenesis. Salmonella, once on the intestinal mucosa, actively multiplies, releasing exo- and endotoxins, causing inflammation. If the body's resistance is insufficient, 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, advanced and chronic.

In carnivores, during the acute course of the disease, an increase in body temperature, lethargy, and decreased appetite are recorded. Vomiting is often noted (especially after eating food), and sometimes there are convulsions with foam coming out of the mouth. Diarrhea then develops, with the feces having a foul odor and containing large amounts of mucus and blood. Puppies quickly lose weight, and the hair near the anus becomes contaminated with feces. Death occurs on the 2-3rd day.

In rabbits and nutria, food refusal and short-term agitation, which turns into a coma, are noted. Body temperature rises to 41–42 °C. Vomiting and diarrhea are sometimes observed. In nutria, in addition, bloody discharge from the nose, convulsions, paralysis of the pectoral muscles, weakness of the rear and profuse salivation are recorded.

In the subacute course, along with signs of pathology of the gastrointestinal tract, respiratory disorders with the development of bronchopneumonia and purulent discharge from the nose are noted in carnivores.

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

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

Pathological changes. When autopsying animal corpses, in the acute course of the disease, the following is discovered:

– hemorrhages in internal organs, on 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 epidemiological 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, where the basis is the isolation of the pathogen and serological identification.

Treatment. Treatment should be comprehensive, including the use of etiotropic, pathogenetic, and symptomatic therapy. Antibacterial drugs should be used taking into account the sensitivity of salmonella to them. Among the specific agents, when treating animals with salmonellosis, polyvalent antitoxic serum is used.

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

timely implementation of forced disinfection, which involves breaking the epizootic chain and preventing further distribution 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. It is mandatory to provide for measures to carry out deratization and disinfection of equipment, care items, and workwear;

disposal of manure and feed residues;

burning of 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, and vircon S should be used.

Carcasses of forcedly killed rabbits and nutria, with good fatness, are used for food after boiling for 1.5 hours. The exhausted ones are disposed of.

A dysfunctional farm (animal farm) is considered recovered from salmonellosis 3 months after the sick animals have recovered, vaccination and final disinfection have been carried out.

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

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

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

Epizootology. Fur-bearing animal puppies and rabbits are most susceptible to pasteurellosis; dog puppies are somewhat less susceptible to the disease.

The source of the infectious agent is sick and recovered animals, as well as pasteurellum carriers, which release bacteria into the external environment with discharge from the nose, exhaled air, saliva, feces and urine. Among pasteurella carriers (there are up to 50% of the herd), the greatest danger is represented 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.

Factors of transmission of the pathogen are poultry meat infected with pasteurels and offal fed to animals in a non-neutralized 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 constant reservoir of pathogens.

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

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 Pasteurella strains in the external environment and which ensures the formation of stationary epizootic foci.

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

Pathogenesis. Virulent strains of Pasteurella actively multiply at the sites of penetration and then penetrate the blood, causing septicemia. The toxins they produce 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 occurs hyperacutely, acutely and chronically. In hyperacute cases, patients die suddenly, without any characteristic clinical signs.

Pasteurellosis in fur-bearing animals, as a rule, is acute and is manifested by severe depression, refusal to feed, unsteady, uncertain gait, and vomiting. Visible mucous membranes are cyanotic (in foxes they are yellow).

Later, diarrhea appears, and sometimes blood is found in the feces. Most often, the phenomenon of hemorrhagic gastroenteritis is recorded in silver-black foxes. In this case, 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 is often acute and is accompanied by loss of appetite, depression, lacrimation and salivation, and vomiting. Body temperature rises to 40.5 °C, ruffled fur, difficulty and rapid breathing, diarrhea, and paralysis of the hind limbs are observed.

The main symptom of nutria pasteurellosis is nosebleeds, which appear shortly before the death of the animals.

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

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

Pathological changes. In acute cases, in carnivores, the following is found:

– 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;

– enlarged spleen;

– catarrhal fibrinous pneumonia (in dogs);

– serous-hemorrhagic lymphadenitis;

in foxes - jaundice.

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

Pasteurellosis must be differentiated from Aujeszky's disease, plague, streptococcosis, and 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 important factor is strict adherence to general preventive measures, as well as veterinary and sanitary rules and preventive vaccination.

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

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

those suspected of being infected are vaccinated. In order to create active immunity, a formol vaccine is used against pasteurellosis in rabbits. An emulsified vaccine is used to vaccinate nutria and mink. In addition, bivalent saponin formol hydroxide-aluminum vaccine against streptococcosis and nutria pasteurellosis, as well as an associated vaccine against botulism and mink pasteurellosis, are used for immunization of animals.

The corpses are burned or disposed of.

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

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

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

Streptococcosis (streptococcosis) is an acute infectious disease characterized in acute cases by sepsis and inflammation of the joints, and in subacute and chronic cases by inflammation of the lungs and intestines. In adult animals, the disease manifests itself as abortion, 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 short chains and stains gram-positive. The size of cocci is 0.5–1.5 microns, they are immobile, do not form spores, and are facultative aerobes.

Streptococcus persists in soil, manure and indoors for 3 weeks, in dried blood and sputum for 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, nutria, rabbits, and dogs are more resistant. More often, the disease is registered in young animals from up to 70 days.

The source of the infectious agent is animals that are sick or have recovered from streptococcosis. The pathogen is excreted from the body through nasal and vaginal discharge, urine and feces.

Factors of transmission of the pathogen include infected food, milk, water, equipment, and bedding. Infection of animals occurs through alimentary and aerogenic routes. The disease occurs more often in the autumn-winter period. The incidence 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 the blood, suppresses phagocytosis and causes septicemia. The released exotoxins destroy the endothelium of blood vessels, increase their porosity, thereby causing profuse 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. Forms of the disease: 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, increased body temperature, conjunctivitis, rhinitis and 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 acute cases, puppies refuse food, become lethargic and inactive. There is an increase in body temperature up to 40 0C, sometimes vomiting, bloody discharge from the nasal openings, diarrhea, 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, and 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, and metritis.

Rabbits with streptococcosis are born with underdeveloped rabbits. Abortions occur 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 autopsying the corpses of dead animals, the following is revealed:

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

– gelatinous infiltration of subcutaneous tissue in the pharynx and torso;

- pulmonary edema;

– hyperplasia of the spleen and lymph nodes;

– liver dystrophy;

in dead dogs:

– catarrhal-purulent mastitis;

– urocystitis, endometritis, vaginitis;

in puppies of fur-bearing animals there are 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, pasterellosis, escherichiosis, Aujeszky's disease, plague, pseudomonosis and gastroenteritis of non-contagious etiology.

Treatment. Hyperimmune serum against streptococcosis is used as a specific treatment. Symptomatic treatment is carried out.

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 prohibited to import animals, feed, cages, etc. from farms unaffected by streptococcosis.

When a diagnosis is made, the farm (farm) is declared unfavorable and restrictions are introduced. A clinical study is carried out daily, patients and those suspected of the disease are isolated and treated.

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

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

Manure and litter are 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 is used against pas terellosis and streptococcosis.

The corpses and fat, after skinning, are burned.

Restrictions from dysfunctional economy removed 15 days after the last case of recovery or slaughter of animals. Final disinfection is carried out.

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 or capsules, is immobile, is located in the form of bunches of grapes, spherical in shape, with a diameter of 0.7–1.0 microns, gram-positive aerobe, actively reproduces on ordinary nutrients environments

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

The source of the infectious agent is female bacteria carriers, as well as sick puppies of the same litter. The pathogen enters the external environment with purulent exudate during the opening of abscesses. Factors of transmission of the pathogen are infected bedding, cages, feed, and care items.

Infection occurs through damaged skin and mucous membranes. This can happen when the female massages the puppy's abdomen with her tongue or when dragging the puppies, when the female grabs him by the skin of his neck. Contributing factors are: unsanitary conditions for keeping animals, the presence of sharp, prickly objects (nails, wire) in cages that lead to skin damage.

There is no pronounced seasonality in the manifestation of enzootic disease, but most often the disease is recorded during the birth of puppies. Pyoderma is characterized by stationarity due to the wide distribution of the pathogen and the presence of animal carriers.

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

Symptoms and course. Mink pups have an incubation period of 24–48 hours. Sick puppies become weaker and stunted 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 have a dark red color 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 become ill much more easily.

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

Pathological changes. Autopsies of dead animals make it possible to establish the presence of abscesses, purulent urocystitis, pyelonephritis and catarrhal-hemorrhagic gastroenteritis.

Diagnosis. The diagnosis is established on the basis of clinical and epidemiological data and laboratory test results. During the diagnostic process, it is necessary to exclude streptococcosis, pasteurellosis, and in rabbits – myxomatosis.

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

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

Antibiotics are injected intramuscularly.

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

its 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.

If a disease appears, a thorough ongoing disinfection is carried out, and after the outbreak is over, a final disinfection is carried out. In permanently disadvantaged farms, where there are real conditions for the occurrence of pyoderma, it is recommended to immunize females with staphylococcal toxoid. It is administered twice in a dose of 0.5 ml on the 10–12th and 15–17th days 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, mobile (monotrich), short, gram-negative, 0.8–1.4 x 0.4–0.6 µm in size. It does not form spores; it is aerobic; when cultivated on solid nutrient media, it forms S-form colonies, which is an indicator of the high virulence of the strain. The pathogen is classified as 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, young Arctic foxes.

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

Transmission factors for the pathogen include 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 through nutritional and aerogenic routes. Wild rodents can be a reservoir of the pathogen, contributing to long-term ill-being.

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

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

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

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

The disease is hyperacute and acute. Characteristic symptoms of the disease appear 1.5–2 hours before death in the form of bloody-foamy discharge 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 aged 2–2.5 months suffer from pseudomonosis, in which diarrhea is recorded, accompanied by the release of feces of a liquid consistency and an unpleasant odor.

In females, shortly before whelping, abortions occur.

Pathological changes. When opening dead minks, the following is revealed:

– 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, epizootological data, the results of a pathoanatomical autopsy with the obligatory microbiological research patmaterial.

The decisive factor is the isolation of a 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 treating sick animals depends on the stage of the infectious process and the selection antibacterial agents. Serum and immunoglobulin are used as specific treatment agents with the simultaneous use of drugs for etiotropic, pathogenetic, symptomatic therapy, as well as drugs that stimulate the body’s protective properties.

Prevention and control measures. When a diagnosis is made, 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 suspected animals. The remaining animals are vaccinated. In order to create active immunity Two 3-month-old minks are immunized with a polyvalent formol aluminum hydroxide vaccine against pseudomonosis. In addition, an associated vaccine is used against viral enteritis, botulism and pseudomonosis;

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

They organize the destruction of rodents, scare away wild birds and take measures to prevent dogs, cats and other animals from entering the farm.

The cage containing sick animals is disinfected using a 2% hot solution of sodium hydroxide or formaldehyde, or a bleach solution (containing 2% active chlorine), or a 1% solution of Vircon C.

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

Organize daily sanitation of workwear, equipment, and care items. The corpses are burned after skinning.

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

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, and nervous disorders.

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

In morphological and cultural terms, leptospires of different serovars are identical and have the appearance of delicate, thin, spiral-shaped rods and threads, with hooked ends, with active movement, 7–14 μm in length. Leptospires are cultivated on liquid elective nutrient media of Ulengut, Lyubashenko, Terskikh, including 5–10% rabbit or sheep 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. Withstands freezing.

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

Animals aged 3–8 months often become ill. However, there are reports that during epizootic outbreaks, leptospirosis is recorded in animals older than two years.

Males get sick more often than females, as they constantly sniff and lick objects that have gotten urine on them.

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 pathogen is released into the external environment through urine, milk, semen, discharge from the genital tract and feces. Transmission factors include infected feed and water sources, bedding and equipment.

The reservoir of the pathogen is mouse-like 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, or when eating the corpses of leptospiron-carrying rodents. Infected water, especially swampy, slow-flowing reservoirs, poses a great danger of the pathogen spreading. In this case, leptospira can enter the body not only through nutrition, 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; epizootic outbreaks are less often recorded. Most often, leptospirosis is diagnosed from May to November and, if it is impossible to break the epizootic chain, conditions are created for the disease to remain stationary. The morbidity and mortality rate of animals is 40–90%.

Pathogenesis. The pathogenic effect of Leptospira is the hemolysis of red blood cells, which causes anemia, accumulation of hemoglobin in the blood and the formation of the pigment bilirubin, which colors the tissues yellow.

Leptospira, once in the kidneys, disrupts their filtering ability, as a result of which hemoglobin appears in the urine. Blood coagulation systems are activated. The capillaries become clogged with bloody clots, which leads to necrosis of large areas of tissue and organs.

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

The hemorrhagic form is characterized by an increase in body temperature to 40.5–41 0C, depression, loss of appetite, dry cracked nose, severe thirst, bad breath, bloody diarrhea or constipation.

Sometimes blood appears in the urine. Muscle pain in the extremities, pain in the abdomen, vomiting mixed with blood, and bleeding from the gums and nasal cavity are almost always recorded. As the disease progresses, intense and sudden weight loss occurs. The skin becomes dry, the eyes become deeply sunken, and the body temperature subsequently drops to 36–36.5 0C. Urine is excreted in small portions and contains yellow pigment and protein. Clonic convulsions appear, with the appearance of which animals can die within a few hours. If the animals survive, they still have paresis, chronic nephritis, and digestive pathology.

The icteric form, caused by L.icterohaemorrhagia, occurs predominantly in puppies and young dogs. At the beginning of the disease, the temperature rises to 40 0C, constipation is recorded, and later the feces soften and become covered with blood. An icteric coloration of the mucous membranes of the eyes, mouth, and individual areas of the skin appears 2–3 days after the disease. With the appearance of jaundice, the animal's temperature drops to 36 0C. Urine is dark yellow with a lot of protein. Itching and conjunctivitis are common.

Pathological changes. When autopsying dead animals, jaundice and congestive hyperemia of the liver, kidneys are found, 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 pathoanatomical changes are taken into account with mandatory laboratory tests.

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

Treatment. When treating 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, routine inspection of breeding stock should be carried out;

examination of blood serum in the RMA of imported animals;

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

If a diagnosis is made, a restriction is imposed. Sick and suspected 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. Deratization is carried out. Prevent the possibility of stray animals 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 is used: the polyvalent vaccine VGNKI against leptospirosis, which is intended for immunization of dogs and fur-bearing animals;

vaccine against canine distemper, infectious hepatitis, adenovirus, parvovirus enteritis and leptospirosis in dogs (hexakanivac);

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

Restrictions are lifted if there are no cases of disease or death of animals from leptospirosis, all veterinary and sanitary measures have been completed, final disinfection has been carried out, and there are no leptospirosis carriers on the farm.

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

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

The spores are highly resistant in the external environment.

Epizootology. Most often, minks and ferrets suffer from botulism, and somewhat less frequently, 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 types of carnivores, from where it enters the external environment with feces, where the spores continue to retain their biological properties for a long time.

Factors of transmission of the pathogen are infected, inferior quality feed; the meat of dead animals, whose carcasses have lain uncut for several hours, is especially dangerous;

corpses of small rodents where toxins have accumulated;

infected meat and fish products.

Infection occurs by eating infected feed raw. Botulism can occur at any time of the year. Enzootic lasts from up 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, stagnation and thrombosis in the capillaries. It disrupts neuromuscular connections, causing muscle relaxation, a decrease in muscle tone, paralysis of the heart muscle, asphyxia and death of the animal.

Symptoms and course. The incubation period lasts from 8 to 24 hours, less often up to 2–3 days. The disease, as a rule, occurs hyperacutely, less often acutely, which is determined by the amount of toxin entering the body.

Sick dogs refuse food, are lethargic, experience increased thirst, and their body temperature is normal. The act of defecation is frequent, the feces are semi-liquid, foul-smelling, 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 have difficulty moving, and a shaky gait is noted. Towards the end of the disease, pulse and breathing become more frequent, urination and defecation slow down, and 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 mobility, the body muscles are relaxed, a sharp expansion of the palpebral fissure and pupil is noted, eyeball protrudes from the orbit of the eye, severe salivation. Subsequently, due to the onset of paresis of the hind or forelimbs, the animals cannot rise to their feet and crawl on their stomachs (Fig. 5.). A sick mink lies prone.

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

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

Shortness of breath is often detected. Some minks report diarrhea and vomiting.

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

Pathological changes. When opening dead minks, catarrhal gastroenteritis, congestive hyperemia of the liver and kidneys, empty intestines and hemorrhages in the pulmonary pleura are revealed.

Diagnosis. The diagnosis is established on the basis of epidemiological data, clinical signs and pathoanatomical changes, with mandatory laboratory tests. The diagnosis is considered established when the causative agent of the disease with characteristic morphological and biological properties is isolated, as well as when botulinum toxin is detected in the pathological material.

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

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

Prevention and control measures. If botulism occurs, suspicious meat and fish feeds are excluded from the animals’ diet or they are fed after careful heat treatment. The same applies to plant feeds that have undergone self-heating and mold.

Particular attention should be paid to the quality of feed after the puppies are weaned and in the first days after vaccination. In order to create active immunity, the following is used: a 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.

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

The fur farm is considered safe after the disease has been eliminated and final disinfection has been carried out.

Tuberculosis (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 is microbes belonging to the genus Mycobacterium. Mycobacterium tuberculosis of human and bovine types causes disease in dogs, cats and fur-bearing animals. In rabbits and minks, tuberculosis is most often caused by mycobacteria of bovine and avian species.

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

Epizootological data. Under natural conditions, silver-black foxes, minks, arctic foxes, nutria, dogs and cats are susceptible to tuberculosis. Nutria and mink are especially sensitive, among which young animals are most often affected. Tuberculosis has not been recorded in sables. In rabbits, the disease is registered mainly in the form isolated cases in the presence of problems with tuberculosis in cattle and birds.

The source of the infectious agent is people with tuberculosis, animals and poultry from whose bodies the pathogen is excreted through nasal discharge, pulmonary sputum, milk, feces and urine.

Factors of transmission of the pathogen can be non-neutralized by-products of animals and birds sick with tuberculosis;

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

In carnivores, nutria and rabbits, the main route of infection is nutrition. Transmission of the pathogen by airborne routes cannot be ruled out. Puppies can become infected during the suckling period from a sick mother.

In sick minks, intrauterine infection of puppies is noted. Animals can become infected through contact 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, having entered the body, penetrates the lungs or other organs, where an inflammatory process develops, manifested by cell proliferation and exudation with the formation of specific tubercle nodules. With a long course of the disease, large tuberculous foci and cavities can form in the lungs, and tuberculous pleurisy develops (especially in dogs and cats). From the lungs, mycobacteria often enter the blood, which leads to the 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, when experimental infection caused by tuberculosis, an allergic reaction develops on days 15-17.

In young minks (puppies 15-20 days old), tuberculosis is malignant, often in the form of generalized damage to internal organs.

In adult minks, signs of the disease appear in the form of deep and extensive lesions in the internal organs. Less common are coughing, nasal discharge, abscesses in the head and neck area, diarrhea, and severe exhaustion.

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

Thus, with pathology of the intestinal tract, vomiting, diarrhea, and severe exhaustion are observed (Fig. 6.).

Rice. 6. Fox sick with tuberculosis.

If the respiratory tract is affected, coughing, wheezing, difficulty breathing, and shortness of breath are noted. If the liver is involved in the process - yellowness of the mucous membranes;

nervous system – agitation, loss of vision, paresis and paralysis of the limbs.

In 5-7 month old fox puppies, it is very common for one or both eyes to be affected. In this case, the eyeball is enlarged in volume, protrudes from the orbit, and clouding of the cornea is observed. After 15–30 days, the eyeball opens and brown liquid flows out of it.

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

Dogs show signs of damage to the lungs (shortness of breath, short, dry cough and nasal discharge) and gastrointestinal tract (vomiting, up to the nose).

In cats, severe emaciation, anemia, difficulty breathing, suppuration of the parotid, submandibular and prescapular lymph nodes are recorded.

The skin and underlying tissues on the head, neck, eyelids, bridge of the nose and cheeks are often 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 revealed);

– focal or diffuse tubercular tuberculous lymphadenitis of the mediastinal, mesenteric and bronchial nodes with the presence of curdled or purulent foci;

– a sharp enlargement of the spleen (8–10 times) with the presence of tubercles;

– tubercular 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 intestines;

– exhaustion;

in foxes and arctic foxes:

– miliary, nodular or nodose tubercles in the lungs;

– tuberculous lymphadenitis of mediastinal and mesenteric nodes;

–presence of small tubercles in the kidneys;

– tuberculous testiculitis (in male foxes);

– exhaustion, anemia and sometimes jaundice;

in nutria:

– miliary or macrofocal tuberculosis in the lungs;

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

– tubercular tuberculosis of mesenteric lymph nodes;

– in some cases, enlargement of the spleen with the presence of tubercles.

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

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

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

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

– for cats in the area of ​​the inner surface of the ear, intradermally in a dose of 0.2 ml;

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

– allergic diagnostics has not found application in rabbits and nutria.

Accounting and assessment of the reaction to tuberculin is carried out in dogs, cats and fur-bearing animals after 48 hours, and animals are recognized as responding when a swelling forms at the site of tuberculin administration.

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 affected lymph nodes and pieces of parenchymal organs and tissues from adult animals are sent to the laboratory.

The diagnosis is considered established when a culture of the tuberculosis pathogen is isolated or when a positive result of a bioassay is obtained.

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

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

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

Prevention and control measures. Once a diagnosis is made, quarantine is imposed. In dog breeding kennels, females with offspring are killed, and their skins are used without restriction. Animals from the unfavorable group are examined for allergies every 60 days until single group negative results are obtained, and after the final veterinary and sanitary measures are taken, quarantine is lifted.

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

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

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 is 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, reproduce by binary fission, contain RNA and DNA, are cultivated on chicken embryos, do not form spores or capsules, and 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, creating a natural reservoir of infection, which contributes to the emergence of secondary foci of chlamydia. They have also been isolated from hares and muskrats. The possibility of interspecies transmission of the pathogen has been established.

Chlamydia most often affects animals between 5 weeks and 9 months of age.

The source of the infectious agent is sick animals and bacteria carriers, as well as animals with a latent form of the disease, which release 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.

Factors of transmission of the pathogen include infected food, water, care items, wool, and overalls.

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

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

Pathogenesis. Having entered the body, the pathogen multiplies in the epithelial cells of the mucous membranes and macrophages. Then it penetrates the blood and is carried into the internal organs, lymph nodes, joints and even into the head and spinal cord, where it causes inflammatory and dystrophic processes.

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

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

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

Pneumonia and diarrhea are subclinical. Abortions and peritonitis are recorded quite often.

Pathological changes. During autopsy of corpses the following is found:

– catarrhal bronchopneumonia;

– serous-purulent conjunctivitis, rhinitis;

– serous-fibrinous pericarditis;

– granular dystrophy of the liver, kidneys and myocardium;

– hyperplasia of the spleen.

Diagnosis. The diagnosis is made comprehensively, taking into account epidemiological data, clinical signs, results of a pathological autopsy and laboratory tests.

The result of the research is considered positive when chlamydia is isolated and identified from the specimen. 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 play a leading role.

Treatment. When providing therapeutic assistance, it should be taken into account that chlamydia is 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, sanitary and zoohygienic rules, the principles of “empty-occupied”, microclimate, and timing of disinfection.

Conducted daily clinical examination, according to the results of which, taking into account serological studies isolate and treat sick animals.

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

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

A farm is considered prosperous if there are no sick animals in it;

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

Dermatophytoses 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 round spots on it, breaking off of hair in the affected areas with subsequent hair loss. Humans also suffer from microsporia.

Etiology. The causative agent of the disease in dogs, cats, rabbits and fur-bearing 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, branched septate mycelium and rounded unicellular spores with a diameter of 2–3 microns 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, Chapek agar, wort agar) at a temperature of 20–30 0C.

Fig.7. Microsporum canis.

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

Epizootology. Microsporia affects cats, fur-bearing animals, rabbits, and dogs. 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 that excrete the pathogen with falling off hair, scales and crusts. A particular danger in maintaining epizootic conditions is posed by stray cats and dogs, as well as rodents (a reservoir of the pathogen). The pathogen can be carried by blood-sucking insects.

Factors of transmission of the pathogen include infected care items, common muzzles, infected feed, bedding, overalls, cages and houses in which sick animals were kept.

Infection occurs directly through contact of sick animals with healthy ones, as well as after feeding offal (heads) from sick animals. Predispose to the disease - high humidity, monotonous diet with a deficiency of microelements 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 increase in incidence in spring and autumn. The disease has a pronounced stationary nature and occurs in the form of an enzootic with population 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 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 hidden (subclinical) forms of the disease. In the vast majority of cases, microsporia occurs in a latent form, sometimes in a superficial form.

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

Rice. 8. Microsporia in mink With a generalized spread of the pathogen, damage to the skin and hair is observed throughout the animal’s body. The spots usually have a round, clearly defined shape. Subsequently, mycotic foci can merge with each other, forming ash-colored crusts. When pressing on the affected areas, purulent exudate appears from the mouth of the hair follicles, which dries out and forms crusts and scabs. (Fig. 8.) The deep form of microsporia is extremely rare; it is recorded in puppies and kittens in the eye area, at the base of the ears, on the forehead and paws in the form of spots with small bubbles and gray-yellow crusts.

In nutrias the disease is accompanied severe itching and can be fatal.

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

The luminescent method involves examining 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 black animals, the glow of the affected hair may be absent. It should be taken into account that rivanol, petroleum jelly and salicylic acid give nonspecific fluorescence.

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

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

3-5% solution of iodine monochloride;

ointment "YAM";

Vaganova ointment;

trichothecin liniment;

15% oil solution of dermaftox;

5-10% phthalan ointment;

5% amikazole ointment;

"Mikozolon" ointment;

ointment "Mikoseptin";

aerosol "Fungiderm";

aerosol "Zoomicol", etc. Along with local treatment, you 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. During the treatment process, it should be remembered that dogs have hypersensitivity to turpentine, and cats to tar, creolin and Lysol.

Vaccines that have a therapeutic and prophylactic effect are used as specific treatments: the inactivated vaccine against dermatophytoses "Polivac-TM" includes 8 species of fungi from the genus Trichophyton and Microsporum;

inactivated vaccine against dermatophytoses "Vakderm";

inactivated associated vaccine against dermatophytoses of carnivores, nutria and rabbits.

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

A farm (farm) where an animal disease has been detected is considered unsafe and restrictions are introduced. Sick and suspected cases are isolated and treated. Crusts, wool, scales are destroyed. All animals are subjected to clinical trial every 10 days and, when sick animals are identified, disinfection is carried out using a hot 2% alkaline solution of formaldehyde.

Manure and litter are disinfected. The overalls are washed twice a week and thoroughly ironed. Persons caring for sick animals must observe the rules of personal hygiene.

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

Restrictions are lifted 2 months after the last case of identifying sick animals and carrying out final disinfection, followed by whitewashing with a 20% slurry of freshly slaked lime.

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

Etiology. The causative agent of the disease is imperfect mold fungi, in the overwhelming majority of cases belonging to the genus Trichophiton mentagrophytes (gypseum) and less commonly Tr.verrucosum. It is cultivated on special nutrient media of Sabouraud, Litman, and wort agar. Spore diameter of Tr.

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

Resistant to freezing, drying, and direct sunlight.

Epizootology. Trichophytosis affects foxes, arctic foxes, dogs, nutria, rabbits and very rarely cats. Animals of all age groups are susceptible, but the disease is most often recorded in young animals. Humans also suffer from trichophytosis.

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

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

Infection occurs through direct contact between sick and healthy animals, as well as through infected environmental objects. Fungal spores can become airborne. The disease in fur-bearing animals can appear after feeding slaughterhouse waste from animals with trichophytosis.

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

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

Pathogenesis. By multiplying in the keratin-rich stratum corneum of the epidermis, the pathogen loosens it, causing inflammation. The hair loses its shine, 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. On the nature of the course and manifestations of the disease serious influence are influenced by housing and feeding conditions, the level of natural resistance and the age of the animals.

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

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. In this case, the deep (follicular) form of trichophytosis is more often recorded, when single foci with exudative inflammation and bursting bubbles form multiple large-sized foci. Intense exudation of the affected areas is accompanied by the formation of dense, thick crusts, which, when pressed, hair follicles, purulent exudate is released. Subsequently, oval and round spots appear, covered with crusts that are difficult to remove. In some cases, there is severe itching in these areas and abrasions soaked in blood can form.

In young nutria, the disease occurs in the form of deep infiltrating 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, torso, and less commonly, limbs. Itching is absent or mild. The number of lesions ranges from 5 to 12. They rise above the surface of the skin by 1–1.5 cm. When the crusts are removed, a bloody-purulent exudate is released at the site of the lesion. Healing of lesions begins from the center and slowly moves towards the periphery.

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

During the diagnostic process, microsporia, scabies, scab, and skin lesions of non-contagious etiology should be excluded.

Treatment. In addition to the means mentioned above, warm 3-5% solutions of iodine monochloride or a 0.25% solution of fish oil or Vaseline oil– trichothecine.

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

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

optimal housing and feeding conditions;

implementation of sa nation premises, sheds and cages.

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

VIROSIS OF FUR ANIMALS Plague of carnivores (febris catarrhalis infectiosa) (infectious catarrhal fever) – acute viral disease, characterized by fever, catarrh of the mucous membranes, pneumonia, skin exanthema and damage to the nervous system.

Bronchopneumonia in adult animals it is characterized by an increase in body temperature by 1-2 ° C, difficulty breathing of the abdominal type (60-80 respiratory movements per minute), pulse - up to 200 beats per minute. The animals lie in the same position, curled up into a ball, their noses are dry, rough, and there is no appetite. The puppies are lethargic, cold on palpation, and squeak. Auscultation reveals popping sounds or wheezing that accompany the act of breathing; the crumbs of the paws are swollen with a purple tint. A blood test reveals leukocytosis with a shift of the neutrophil nucleus to the left, a reduced number of red blood cells and hemoglobin content.

For therapeutic purposes, antibiotics are used intramuscularly: penicillin, Bicillin, monomycin, tetraolean, sulfonamide and others antibacterial drugs. Prevention is aimed at using all the rules of technology for feeding, caring for and preserving fur-bearing animals and conducting routine medical examinations of them.

Gastroenteritis characterized by decreased or absent appetite, vomiting, depression and diarrhea. Feces are unformed, liquid, with mucus of different colors (gray, light pink, green or brown). Hemorrhagic gastroenteritis develops very quickly and is accompanied by profuse diarrhea with mucus and blood. Sometimes vomiting of bloody fluid or feces that resemble tar in color and consistency are observed. They show cyanosis and anemia.

For therapeutic purposes, acidophilus, ABA, bacteria, antibiotics (tetracycline, neomycin, erythromycin, streptomycin, tilan) in combination with nitrofuran (furazolidone, furadonin) and sulfonamide drugs (tribrisen, oriprin, metacrine) are added to the feed. Symptomatic agents are used (glucose, camphor oil, protein hydrolysates, saline solution). Prevention is aimed at controlling the quality and quantity of feed, their storage regime, and providing vitamin and mineral supplements.

Hepatosis. Fur animals mild form look clinically healthy. They experience a decrease in resistance, abortions, and the birth of still and non-viable puppies. Blood is found in the urine. The coat loses its shine and has a reddish or brown tint. Dysuria, convulsions, and seizures develop. In severe forms, they exhibit loss of appetite, weight loss, anemic or yellowishness of the visible mucous membranes and skin (lips, nose, crumbs of fingers), depression, nervous disorders - convulsions and paresis of the limbs. Feces are poorly formed, with mucus, sometimes resembling tar in color and consistency.

For individual treatment, lipotropics and hematopoietic drugs, vitamins, amino acids, electrolyte solutions, and symptomatic therapy are used. Prevention is aimed at organoleptic and laboratory control of the quality of feed, the rules of feeding them, the level of total and complete protein and the provision of multivitamin supplements (Pushnovit-1 Pushnovit-2, Polfamyxin). Group diet therapy and dietary prevention are recommended.

Toxemia of pregnant women characterized by depressed animals and lack of appetite. Over time, involuntary muscle contractions and coma occur. Animals die in last stage pregnancy.

For therapeutic purposes, sick animals are given oral vitamin B, 2, folic acid, vitamin E. It is effective to feed the liver and its preparations. Pushnovit-1 or pushnovit-2 is used. Prevention is aimed at avoiding feeding rancid fats and giving multivitamins and microelements. For individual treatment, lipotropin and hematopoietic drugs, vitamins, amino acids, electrolyte solutions, and symptomatic therapy are used.

Urolithiasis disease. Examination reveals growth retardation and loss of appetite. Over time, hematuria, urinary colic, uremia, and frequent painful urge to urinate appear. Animals walk with widely spaced pelvic limbs. When the urethra is blocked, palpation reveals an increase in the volume of the abdomen as a result of paralysis of the bladder.

The radical treatment method is surgery. It is recommended to prescribe ammonium chloride, orthophosphoric acid, and feed nettles. Hexamethyltetramine, streptocide, phenyl salicylate, sodium bicarbonate, cystenal are used with food. Prevention is aimed at normalizing acid-base balance and mineral and vitamin metabolism.

Nutritional (iron deficiency) anemia. Inspection reveals anemia in the visible mucous membranes, down-free areas of the skin, the crumbs of the paws and nose. Appetite decreases, animals lose weight, are stunted and die. When examining blood, the hemoglobin level decreases depending on the course of the disease. In puppies that survive, the undercoats become depigmented (bilopurosis). A study of sick females reveals their weight loss, loss of maternal instinct, the birth of dead, anemic or small puppies with impaired digestive function, low hemoglobin in the blood.

For therapeutic purposes, feroglucin, ferodex, and other organic iron preparations are administered at a dose of 0.5-1 ml/kg body weight. Glucose, vitamins B] 2, C, A, protein hydrolysates are shown. Prevention is aimed at introducing into the diet a group of feeds containing iron compounds and iron-containing preparations (feroglzhin, ferroanemine, ferrous sulfate, ferrous glycerophosphate, ferrous lactate, ferric glutamate (Chemax)).

A-hypovitaminosis. Animals exhibit conjunctivitis, xerophthalmia, and decreased vision. In females, the reproductive function is disrupted or weak, non-viable offspring are born. Nervous phenomena are observed in puppies: twitching, head throwing, circular movements, lame gait.

For therapeutic purposes, vitamin A and multivitamins are prescribed internally. Prevention is aimed at providing fur-bearing animals with feed and feed additives containing vitamin A. Vitamin A and multivitamins are prescribed in preventive doses.

B-hypovitaminosis. Examination reveals growth retardation in puppies. Sometimes they have attacks of tetany. Palpation reveals thickening of the joints and costal “rosaries”. Over time, the diaphysis of the bones of the forearm, shoulder, lower leg, and thigh become bent.

For therapeutic purposes, calciferol, bone meal, ultraviolet irradiation, and multivitamins are prescribed. Prevention is aimed at adequate feeding and the introduction of mineral and vitamin supplements. Effective photoprophylaxis.

C-hypovitaminosis characterized by swelling of the paws in puppies. The paws are swollen, the joints are thickened, the skin is tense. Eczema develops between the toes and the skin becomes red (red feet). Puppies squeak, constantly move, hunch over, throw their heads back, and do not attach well to their mother's nipples. They die within 4-5 days of life. In adult animals, anemia, ulcerative stomatitis, joint pain, and nosebleeds are observed.

IN medicinal purposes Prescribe ascorbic acid, pushnovit, vegetables. For prevention, the diet includes foods rich in vitamin C and multivitamins.

Diseases of the skin of fur-bearing animals lead to a decrease in value, and sometimes to a complete depreciation of the fur skin. Therefore, the study of these diseases and the fight against them is of great economic importance. In this article we will talk about diseases of the fur of mainly wild fur-bearing animals.

In foxes under natural conditions, damage occurs in most cases by causative agents of equine scabies. The body of this tick reaches a length of 0.2-0.5 millimeters. On the dorsal surface there are scaly outgrowths and bristles directed backwards with their tips. The proboscis is horseshoe-shaped. The legs are thick and short.
Ticks spend their entire lives in all stages of development on the host's body. They live in the thickness of the skin and feed on lymph, making winding passages in the epidermis. Females lay from 20 to 50 eggs, from which larvae hatch after three to seven days, turning into nymphs after three to four days. After two molts, mature ticks are formed from the nymphs. The full development cycle of the itching mite takes 15-20 days.
Sick animals serve as sources of infection. Infection occurs through contact with sick people or through care items, cages and houses that sick animals have come into contact with. Under natural conditions, infection with horse itch mites occurs when foxes and wolves eat the corpses of horses affected by scabies.
Initially, in foxes and arctic foxes with scabies, the paws, inner thigh area, root of the tail and head are affected. In the future, the process can spread to the entire surface of the skin. Small nodules form on the affected areas, turning into blisters. As a result of scratching, a secretion is released from the affected areas, which, when dried, forms crusts. The fur falls out, and in areas with thick hair it falls off. The animal loses its appetite, loses weight and often dies.

To eliminate the epizootic, in some places it is advisable to destroy all sick foxes. Their burrows should be treated with a sharp-smelling acaricidal agent (creolin) and then buried. This measure is very labor-intensive, but necessary for the improvement of some areas where the disease of scabies is very common.
Treatment of dogs and caged fur-bearing animals affected by scabies is carried out with various mite-killing agents, of which the most effective is sulfur dioxide. They fumigate sick animals in special chambers two to five times with an interval of six to seven days, depending on the severity of the lesion. The head is treated with some solution, for example, a soap suspension of hexachlorane - 0.3-0.5 percent, soap “K” or sulfur-creolin liniment. The same means can be used to general treatment.
First, dirt and crusts are removed from the surface of the skin of a sick animal using warm water, preferably with green soap.

In order to determine the presence of these mites, a deep scraping is taken from the affected areas of the skin, preferably from the contents of the pustules.
By analogy with dogs, which can also become infected from sick animals, the best treatment should be considered intravenous administration of a one percent solution of trypansinia or methylene blue at a dose of 0.01 grams per kilogram of live weight, repeated two or three times at weekly intervals. .At the same time, rub finely dispersed sulfur into the skin of the affected areas. In addition, they use carbon tetrachloride, Peruvian balsam, iodine tincture, DDT, “K” soap, etc.
In order to prevent and eliminate sources of infection, sick and suspected dogs, and in fur farming, animals are isolated and treated. Cages, houses and equipment are disinfected with a blowtorch.
Infectious dermatitis of fur-bearing animals. The causative agents are staphylococci and streptococci. Rodents are mainly susceptible to this disease: squirrels,
chipmunks, pikas, hares.
As is known, the pathogenic significance of staphylococci and streptococci is explained, on the one hand, by their ability to secrete toxins, enzymes and other biologically active products that disrupt the vital functions of affected animals, and on the other hand, by their resistance to the body’s defenses.

Staphylococci and streptococci are common inhabitants of the surface of the skin of animals and especially rodents, but undamaged skin is a fairly powerful barrier for them. Preceding injuries and inflammatory processes are very important in the development of infection. The weakening of the body’s protective properties, for example, during fasting, severe infestations and vitamin deficiencies, is also of great importance.
According to our observations, in some years streptococci and staphylococci can be pathogenic for predators, especially the mustelid family, if their body is severely weakened. Contamination of the surface of the skin of predators with streptococci and staphylococci occurs when they catch infected rodents, which serve as their usual food.
Currently, the most widespread opinion is that its adherents classify staphylococci as potentially pathogenic microbes. The latter can exist at the expense of the tissues of dead animals, but with the emergence of conditions that contribute to the weakening of the host’s body, which were mentioned above, they penetrate into a living organism, adapt to nutrition at the expense of its tissues and increase their virulence, becoming pathogenic. Such weakening conditions are severe hunger strikes, infections and infestations, including helminthic ones.

When externally examining the carcasses of sick animals, areas of skin that appear to have clipped fur are striking. Hair is brittle and falls out, hair follicles are thickened and necrotic.
If the skin is severely damaged, dark spots of various sizes, which sometimes merge to form large areas. The mesra at the site of the spots is thickened and sometimes there are fistulas with swollen edges and pus discharge. The latter glues the fur together, forming crusts, which, when separated, cause ulcers. When the ulcers dry, scabs form at the site of the ulcers. With severe damage, the skins are completely worthless. The disease has been extremely poorly studied.
K. MALYSHEV, Candidate of Veterinary Sciences