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Tularemia. The causative agent of the disease, epizootic data, the course of the disease in farm animals, the course and symptoms of the disease, pathological changes, diagnosis, prevention and control measures, prevention of commercial infections, treatment

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Tularemia is a naturally focal, transmissible infection, which affects most mammals

Tularemia is a naturally occurring, vector-borne infectious disease that affects most mammalian species, including birds and humans. This disease has not spared cats either. The disease manifests itself in fever, septicemia, inflammation of the intestinal mucosa and upper respiratory tract. In addition, there is an increase and cheesy degeneration of regional lymph nodes (or lymphadenitis). In addition, various inflammatory-necrotic foci appear in the lungs, liver and spleen, paralysis, the nervous system is affected, and the animal loses a lot of weight.

The causative agent of tularemia exhibits significant resistance in external environment, especially when low temperatures, but at the same time it is very sensitive to various physical (sun, ultraviolet rays, ionizing radiation, high temperature) and chemical influences.
This disease first struck Tulare County, which is located in the state of California (USA) in 1908. Rodents were the first to become ill. And in 1911, McCaw and Chapin identified the culture that caused the disease. In 1921, sheep and people suffered from the same disease in the same US state. At the suggestion of E. Frenisis, the disease was named tularemia. This disease is common in America, Japan, certain countries of Europe and Asia, as well as in Africa. In other words, most people suffer from tularemia, as a rule, in countries whose climate is moderate and even. Northern Hemisphere. In Russia, this disease was first discovered in 1921. From an economic point of view, the damage to livestock caused by tularemia is generally insignificant, because clinical form the disease is extremely rare. Only carrying out anti-tularemia measures causes material damage, as it requires significant waste.
The causative agent of this disease is Francisella tularensis, which in turn is divided into three species - American - Francisella tularensis nearctica, Central Asian - Francisella tularensis mediasiatica, and European-Asian - Francisella tularensis holarctica. Euro-Asian can also be Holarctic and Palearctic. IN Russian Federation for example, the Holarctic species is mainly widespread.
In an animal organism, this disease, its microorganism, manifests itself in the form of thin, short rods that are static, do not form spores and have a capsule. Under aerobic conditions on specially designed solid or liquid nutrient media, it begins to be cultivated. Cultivation also occurs in chicken embryos, thereby causing their death within 70-120 hours after infection.
If avirulent species contain only O-antigen, then virulent species include O-, H- and V-antigens.

Epizootology
One hundred and twenty-five species of vertebrates and one hundred and one species of invertebrates are predisposed to tularemia. In their natural habitat, hares, water rats, mice, wild rabbits, hamsters, beavers, chipmunks and muskrats can become ill. Cases of the disease have also been reported in various species of birds. Natural foci of the disease can be active for more than fifty years. As for farm animals, the most susceptible to the tularemia virus are piglets and lambs aged two to four months, as well as cattle, donkeys and horses. In addition, camels, rabbits, reindeer and buffalo can suffer from this disease. If we consider resistance to the disease, it turns out that young sheep are more likely to become infected with this disease than older individuals. At the same time, the immunity of goats against tularemia works much better than that of sheep. As for birds, chickens, especially small chickens, are at risk. But turkeys and geese are practically unable to become infected. If we take laboratory animals, the most susceptible to the disease are white mice and guinea pigs.
The main source of the disease is infected animals. For tank in environment serve populations of the above-mentioned species of wild animals. The virus is transmitted by infected food, reservoirs and soil, as well as blood-sucking insects.
There are three ways in which domestic and farm animals, if included in the so-called epizootic process, which usually occurs among wild animals, can become infected in three ways:
- nutritional;
- aerogenic;
- transmission.
It should be noted that the virus can enter the body through intact skin, as well as the mucous membrane of the respiratory organs and the conjunctiva. Moreover, sometimes infection occurs as a result of prenatal consumption of infected animals. So, for example, cats and pigs can become infected by eating rats and mice, but what about dogs? rabbits and hares. In other words, their objects for hunting.
Farm animals cannot transmit the virus within the herd because their disease is latent and the bacteria are shed passively. That is, farm animals take absolutely no part in the blood circulation of the pathogen.
Tularemia outbreaks are also distinguished by seasonal differences:
pasture, which occurs in the spring-summer period;
stall? falls in the autumn-winter period.
This division is associated with the activity of blood-sucking insects in different seasons, as well as with places where food is stored and the presence of rodents in camps.

Pathogenesis of Tularemia in cats
As soon as the virus enters the animal’s body as a result of the bite of an arthropod or rodent, with food, water or air, the process of its spread immediately begins at the site of introduction. After this, the infection reaches the regional lymph nodes. There it continues the process of its reproduction, thereby causing a purulent-inflammatory process. This leads to an increase lymph nodes, their hardening, subsequent softening and opening. The tissue that surrounds the site of infection swells and becomes hyperemic. As a result, microbes from infected nodes penetrate the blood and spread throughout the body, which leads to damage to other lymph nodes in the lungs, liver and spleen, and the formation of new ulcers. Parenchyma cells are affected, and the development of septemia begins. The animal dies when the concentration of microbes in its body reaches its maximum.
How does the disease progress? Its clinical manifestation. You can suspect that there is an epidemic of tularemia among wild animals by their behavior. Their instinct of self-preservation weakens. For example, hares and wild rabbits cease to be afraid of humans and allow them to easily catch themselves. Mortality among rats and mice increases.
Dogs affected by tularemia may lie motionless for hours, lose their appetite, and increasingly hide from the sun in the shade. Animals also experience severe emaciation, the conjunctiva becomes covered with numerous ulcers. Especially if we're talking about In sick dogs, the inguinal and mandibular lymph nodes become enlarged. In addition, paralysis and cuts to the hind limbs are observed. It also happens that illness leads to disorder digestive system. And when the disease begins to come to an end, the animals suddenly begin to feel weak, the heart reduces the activity of its activity, and anemia of the mucous membranes occurs. As for cats, they become flabby, the lymph nodes on their neck and head swell, then vomiting, emaciation and eventually death begin.

Pathological signs of tularemia in cats and kittens
The bodies of dead animals show emaciation, and baldness is observed in the axillary area. On certain parts of the body, compactions are noticeable, which are covered with hemorrhages and necrosis, the lymph nodes are enlarged and covered with many ulcers. The pharynx is enlarged: the tonsils and the root of the tongue are clogged with caseous-purulent plugs. The spleen swells, and when cut, the pulp becomes dark red in color, and the nodules become gray-yellow. As for the epicardium and adrenal glands, pinpoint hemorrhage forms on them. In a word, based on the overall picture, we can talk about sepsis.
In rodents, pathological signs are similar to those of pseudotuberculosis.

Diagnosis and differential diagnosis of Tularemia in cats and cats
Tularemia is suspected when it is present in humans, rodents, as well as farm and domestic animals. The diagnosis can only be made when the following studies are carried out:
clinical symptoms;
epizootic and pathological data;
bacteriological;
serological: RA, RP, RIGA, RN;
allergic: tularin is administered subcutaneously.
In order to determine the presence of the disease in a corpse, an antibody erythrocyte diagnostic test is performed.
To conduct a bacteriological study, you must send it to veterinary clinic rodent corpse. As for large animals, it will be enough to send their liver and spleen, as well as kidneys, affected lymph nodes and heart for research. Next, parts of the body are subjected to bacterioscopy, seeding is done, and the isolated cultures are identified by antigenic, cultural-morphological and biochemical properties.
After conducting a bioassay of the isolated culture, suspensions from lymph nodes and pieces of organs, laboratory animals are infected, most often white mice. Next, animals are observed, experimentally infected, and they die on the third or second day from the moment of infection.
As a result, the following pathological settings are considered:
1. isolation of F. tularensis culture from pathological material.
2. in the case when the biosample is pure, but changes in the body characteristic of tularemia are found in it, isolating a pure culture from it.

Immunity, specific prevention of Tularemia in cats

After the animal recovers, its immunity decreases significantly. Antibodies are formed in their blood, and sensitization of the body also begins. As for vaccinating animals, it makes no sense to carry it out, since the vaccine that is vaccinated against tularemia in people does not actually work on animals.

Prevention of tularemia in cats
The most common measure in the fight against this disease is the destruction of the source of the disease, neutralization of water, food, etc. For example, reducing the number of ticks leads to a reduction in the risk of disease in livestock during grazing. In other words, the destruction of carriers and pathogens of the disease leads to the fact that the likelihood of becoming infected is reduced to almost zero. Cattle are also grazed on artificial meadows and pastures, destroying natural ones.
Rodents are disposed of by pressing straw and hay into bales and then treating them with ammonia. It is also necessary to ensure the safe transportation of haystacks and straw sweeps and their subsequent storage in areas where rodents cannot enter. Under no circumstances should you leave straw and hay on the edges of forests and ravines.
Treatment. Currently not developed yet special remedy for the treatment of tularemia. Therefore, antibiotics such as streptomycin, chloramphenicol, dihydrostreptomycin, oletethrin, tetracycline, chlortetracycline, as well as sulfonamide and nitrofuran drugs are used here.

Measures to protect public health
Prevention of the disease among people in the territory of the outbreak of the disease involves sanitary measures and epizootological and epidemiological examination of the outbreak. The procedure for hospitalization of patients and their clinical examination must also be followed. And of course, the state of antitularemia immunity was monitored as carefully as possible.

1.9. Tularemia in animals

Tularemia(Latin - Tularemia; English - Tularaemia) - natural focal, transmissible infectious disease mammals of many species, birds and humans, manifested by septicemia, fever, damage to the mucous membranes of the upper respiratory tract and intestines, enlargement and cheesy degeneration of regional lymph nodes (lymphadenitis), the appearance of inflammatory-necrotic foci in the liver, spleen and lungs, emaciation, mastitis, abortions, defeat nervous system and paralysis.

Historical background, distribution, degree of experience A damage and loss. The disease was first discovered in 1908 in Tulare County (California, USA) in rodents. McCaw and Chapin (1911) were the first to isolate the culture of the pathogen. Then, in the same US state, the disease was discovered in people and sheep (1921). E. Francis proposed to call it tularemia. Tularemia is recorded in North America, Japan, various countries of Europe, Asia and Africa. The disease is distributed mainly in temperate landscapes climate zone Northern Hemisphere. In our country, it was first registered in 1921. The economic damage caused by tularemia to livestock is generally insignificant, since clinically pronounced disease is rare in farm animals. However, anti-tularemia measures require large expenses.

The causative agent of the disease. The causative agent of tularemia is Francisella tularensis. Within species F. tularensis, according to their geographical distribution, three subspecies are distinguished: Nearctic, or American (F. t. nearctica), Central Asian (F. t. mediasiatica) and Holarctic, or Euro-Asian, Palearctic (F. t. holarctica). The latter, in turn, includes three biovariants. The Holarctic subspecies F is widespread on the territory of the Russian Federation. tularensis subsp. holarctica (with two biovars I Ery^ and II Ery R).

In the body of animals, the microorganism is found in the form of short thin rods, does not form spores, has a capsule, and is immobile. Cultivated only under aerobic conditions on special liquid or solid nutrient media (MPB with cysteine ​​and glucose, coagulated whey, MPB with cysteine ​​and blood, medium with yolk chicken egg etc.), as well as in 14-day chicken embryos, causing their death 72...120 hours after infection.

Virulent varieties contain O-, H-, V-antigens, while avirulent varieties contain only O-antigen.

The causative agent of tularemia exhibits significant resistance in the external environment, especially at low temperatures, but at the same time it is very sensitive to various physical (sun, ultraviolet rays, ionizing radiation, high temperature) and chemical influences.

Epizootology. 125 species of vertebrates and 101 species of invertebrates are susceptible to tularemia. IN natural conditions Tularemia mainly affects hares, wild rabbits, mice, water rats, muskrats, beavers, hamsters and chipmunks. Cases of disease in birds of various species have been reported. Natural foci can be active for 50 years or more. Of the farm animals, they are most sensitive to the causative agent of tularemia and can become clinically ill. pronounced signs diseases of lambs and piglets under the age of 2...4 months, cattle, horses and donkeys. Buffalo, camels, reindeer and rabbits are also susceptible to infection. Adult sheep are more resistant than young animals, and goats have higher resistance compared to sheep. Of the poultry, chickens (especially chicks) are the most susceptible. Turkeys, ducks and geese are highly resistant to infection. Dogs and cats are less susceptible to the pathogen. Among laboratory animals, guinea pigs and white mice are the most susceptible.

The main source of the pathogen is sick animals. Its reservoir in the environment is the population of the above-listed species of wild animals, and its transmission factors are blood-sucking insects, infected water sources, feed and soil.

Infection of agricultural and domestic animals when they are included in the epizootic process occurring among wild animals occurs mainly through nutritional, aerogenic and vector-borne routes. Bacteria can enter the body even through intact skin, conjunctiva and mucous membranes of the respiratory system. Intrauterine transmission of the pathogen is possible. Dogs usually become infected by eating infected carcasses of hares and rabbits (hunted objects), and cats, like pigs, by eating the corpses of rats and mice.

Due to predominantly latent (asymptomatic) manifestations of the disease, insignificant contamination of organs, absence of active bacterial excretion, farm animals do not participate in the circulation of the pathogen, therefore, there is no mutual re-infection within the herd.

Outbreaks of tularemia are observed both in the spring-summer (pasture) and in the autumn-winter (stall) periods, which is associated, respectively, with increased activity blood-sucking insects and more intensive migration of rodents to livestock buildings and feed storage areas in certain seasons of the year.

Pathogenesis. Once in the animal’s body through food, water, air, or through bites from blood-sucking arthropods and rodents, the pathogen begins to multiply at the site of introduction. Then it is transported through the lymphatic ducts to the regional lymph nodes, where, continuing to multiply, it causes a purulent-inflammatory process. This process is accompanied by a significant increase in the size of the lymph nodes, their hardening, and then softening and opening. The surrounding tissue is hyperemic and edematous. From the affected nodes, microbes quickly penetrate into the bloodstream and spread through the bloodstream (bacteremia) throughout the body, settling in other lymph nodes, spleen, liver, lungs, etc., causing the formation of new pustules and damage to parenchyma cells (septicemia develops ). Animal death occurs from intoxication when the concentration of bacteria in the blood reaches the terminal phase.

Course and clinical manifestation. Suspicion of tularemia in wild animals is usually caused by the increasing number of deaths of rats and mice. Sick hares, wild rabbits and squirrels lose their natural fear of humans, do not flee and allow themselves to be easily caught.

The incubation period for tularemia in farm animals (sheep, goat, pig, horse) lasts from 4 to 12 days. Depending on the species, breed and age of the animal, the disease can be acute, pre-acute or chronic, manifest in a typical or atypical (erased, latent, asymptomatic, innaparent) form.

In sheep acute course a depressed state is usually observed: adult sheep and lambs stand with their heads bowed or lie down, reacting weakly to external stimuli. When grazing, they lag behind the herd. The gait is unsteady, the pulse is accelerated (up to 160 beats/min), breathing is rapid (up to 96 per 1 min). Body temperature rises to 40.5...41 °C. It stays at this level for 2...3 days, then drops to normal and rises again by 0.5...0.6°C.

In sick lambs, relaxation and paresis of the hind limbs, diarrhea and pallor of the mucous membranes (anemia due to a decrease in hemoglobin concentration to 40...30 g/l when the norm is 70...80 g/l), catarrhal conjunctivitis and rhinitis, accompanied by serous mucous discharge from the nose. The mandibular and prescapular lymph nodes are enlarged, dense, and painful. As the disease progresses, except specified symptoms severe anxiety and extreme agitation are observed. During this period, some animals develop paralysis, then a coma sets in and the patients die within the next few hours. The disease lasts 8...15 days. The morbidity rate in lambs is 10...50%, and the mortality rate is 30%.

Tularemia in adult pigs often occurs latently. In piglets 2...6 months of age after an incubation period of 1...7 days, the disease is manifested by an increase in body temperature to 42 °C, refusal to feed, depression, rapid abdominal breathing and cough. Observed profuse sweating, causing the skin to become dirty and crusty. Lymph nodes are enlarged. The high body temperature is maintained for 7...10 days, and if there are no complications from the respiratory system, a slow recovery begins. Otherwise, progressive emaciation is observed in sick animals. Most of them die.

At the large cattle The disease in most cases occurs without visible clinical signs (asymptomatic) and is detected only by serological research methods. In some cases, sick cows experience short-term fever, swollen lymph nodes and mastitis. Abortions are possible in pregnant animals (50 days after infection). General state and appetite remain unchanged. Cases of manifestation of the disease in the form of paralysis of the limbs with fatal outcomes have been described.

In buffaloes, during experimental infection, it was observed loss of appetite, chills, cough, rapid breathing and enlarged regional lymph nodes.

In camels the main clinical signs illnesses are chills, cough, significant fever, rapid breathing, enlarged subcutaneous lymph nodes and loss of body condition.

With tularemia infection in horses, mild and asymptomatic forms of the disease are observed, detected by allergic and serological tests. Under conditions of natural infection, tularemia in mares usually manifests itself as mass abortions in the 4th...5th month of pregnancy without any subsequent complications. Body temperature remains normal. In donkeys, body temperature rises by 1...2 °C and remains at this level for 2 weeks. Anorexia and exhaustion are observed.

Adult chickens, pheasants, and pigeons often become ill asymptomatically. Under natural conditions, young chickens experience a decrease in fatness, the appearance of inflammatory foci and the accumulation of caseous masses in the area of ​​the root of the tongue and pharynx.

In domestic rabbits, the disease is often asymptomatic (hidden), manifests itself atypically and clinical signs may be similar to staphylococcosis, pseudotuberculosis and chronic pasteurellosis. In typical cases, they have rhinitis, abscesses of the subcutaneous lymph nodes and emaciation. The disease can last from 5...6 days to 1 month or more. Most animals die.

Tularemia infection in dogs occurs with extremely varied clinical signs. Sick animals show a depressed state (they are lethargic, hide in the shade, lie motionless), loss of appetite, severe weight loss, and mucopurulent conjunctivitis. A characteristic sign for sick dogs is enlargement of the inguinal, popliteal and mandibular lymph nodes. Paresis and paralysis of the hind limbs are noted. Sometimes the disease is accompanied by signs of severe dysfunction gastrointestinal tract. Towards the end of the disease appear severe weakness, decline in cardiac activity, as well as severe anemia of the mucous membranes. Cats experience laxity and swelling of the regional lymph nodes of the head and neck, vomiting, emaciation and death.

Pathological signs. The corpses of dead animals are exhausted. The skin in the axillary area is ulcerated and necrotic. Under the skin and in the subcutaneous tissue of various parts of the body, compacted areas with hemorrhages and foci of necrosis are found. The mandibular, retropharyngeal, prescapular and axillary (and if the course is prolonged, internal) lymph nodes are enlarged and purulently inflamed. The nasal mucosa is swollen and hyperemic. The pharynx is hyperemic; at the root of the tongue and in the tonsils caseous-purulent plugs. In addition, fibrinous pleurisy and focal serous-fibrinous pneumonia, congestive hyperemia and necrotic foci in the liver are found in lambs and piglets. The spleen is swollen, its pulp on a section has a dark red color and serous-yellow nodules. There are pinpoint hemorrhages on the epicardium and adrenal glands. The overall picture of sepsis is created.

Pathological signs in rodents are similar to the changes observed in pseudotuberculosis.

Diagnosis and differential diagnosis. Suspicion of tularemia arises in the presence of this disease in rodents (mass mortality), diseases of farm and domestic animals, as well as humans. The diagnosis is made based on the analysis of epizootic, clinical, pathological data, taking into account the results of bacteriological, serological (RA, RP, RIGA, RN) and allergic (intradermal administration of tularin) studies. To determine the antigen in animal corpses, an antibody erythrocyte diagnosticum is used.

For bacteriological examination, whole corpses of rodents and small animals are sent to the veterinary laboratory, and from the corpses of large animals - the liver, kidneys, spleen, heart, and affected lymph nodes. In a veterinary laboratory, bacterioscopy is carried out, cultures are made from pathological material, followed by identification of the isolated cultures by cultural-morphological, biochemical and antigenic properties.

In a bioassay, guinea pigs or white mice are infected with an isolated culture, a suspension of pieces of organs and lymph nodes, and, if necessary, the material is examined in a precipitation reaction. In guinea pigs experimentally infected during a bioassay (whose death is noted after 2...3 days), pathognomonic changes are considered to be inflammation and the formation of ulcers at the site of introduction of the biomaterial (or culture of the pathogen), suppuration of regional lymph nodes, enlargement of the spleen and liver, nodular and focal lesions in the lungs. White mice die on the 3rd...4th day after infection. Their diagnostic signs are a clay-colored liver, an enlarged spleen with gray-white nodules.

According to the results laboratory research the diagnosis is considered established:

when isolating a culture of F. tularensis from the sent pathological material;

with a positive bioassay with changes in organs characteristic of tularemia and subsequent isolation of a pure culture from them.

At differential diagnosis tularemia should be distinguished from anaplasmosis, pseudotuberculosis, tuberculosis, paratuberculosis, brucellosis and coccidiosis (eimeriosis) by conducting bacteriological, serological and allergic studies.

Immunity, specific prevention. After recovering from the disease, the animal develops intense immunity. Antibodies are detected in the blood of re-convalescent animals, and sensitization of the body occurs. Proposed for immunization of people against tularemia live vaccine When administered to animals, it turned out to be weakly immunogenic, so animals are not vaccinated.

Prevention. In the system of preventive measures, one of the first places is occupied by measures to neutralize the source of the infectious agent, transmission factors and carriers of the pathogen. The reduction in the number of ixodid ticks is facilitated by a change in the timing (late start) of spring grazing, a reduction in the area of ​​natural meadows, grazing on artificial and cultivated pastures, and planned or emergency treatments of tick-infested livestock.

Reducing the number of rodents is achieved by pressing hay and straw into bales; high-quality treatment of haystacks and straw sweeps with ammonia, transportation of feed immediately after harvesting to well-equipped storage facilities that rodents cannot penetrate. It is not recommended to install haystacks and straw sweeps along the edges of ravines or forest edges.

Treatment. Specific treatments have not been developed. Sick animals are treated with antibiotics (streptomycin, chloramphenicol, dihydrostreptomycin, oletethrin, tetracycline, chlortetracycline), sulfonamide and nitrofuran drugs.

Control measures. Sick animals are isolated and treated. The slaughter of sick and disease-suspicious animals for meat, as well as the skinning of them, is prohibited. In the case of slaughter of sick animals, carcasses along with organs and skin are destroyed. Slaughter products obtained from healthy animals of a dysfunctional herd and contaminated with rodent droppings are cleaned and sent for the production of cooked sausages (at a local enterprise).

The export of animals from unfavorable farms is permitted after testing blood serum in an agglutination reaction and treatment against pasture ticks.

Measures to protect public health. Measures to prevent human diseases on the territory of the epizootic outbreak in accordance with sanitary rules provide for an epizootological and epidemiological examination of the outbreak; hospitalization procedure and dispensary observation; immunoprophylaxis; monitoring the state of anti-tularemia immunity and familiarizing the local population with measures to prevent infection during different types works

Test questions and assignments. 1. Describe the main pathogens and geographic distribution of the disease. 2. What animal species are the reservoir of pathogens and what determines the natural focality of tularemia? 3. What are distinctive features epizootic and epidemic processes in this disease? 4. The course and forms of clinical manifestations of tularemia in wild and farm animals. 5. What measures need to be taken to eliminate reservoirs of pathogens and prevent infection of farm animals in areas of stationary epizootic tularemia foci?

Tularemia(Tularaemia) is a natural cell disease of wild rodents, fur-bearing animals, farm and domestic animals, which is accompanied by hemorrhagic septicemia and paralysis in young animals, abortions in adult animals. People get sick with tularemia.

Historical reference. The disease was first discovered by Mack Creativity and Chapin (1911) among wild ground squirrels in California, in the province of Tulare, from where it got its name. In our country, a disease similar to tularemia among people was observed in the Volyn province back in 1825 by N.K. Chornobaev. During the First World War, epidemics of tularemia were described under the name “Volyn” or “trench fever.” S.V. Suvorov, A.A. Wolfertz and M.G. Voronkova (1926) obtained a pure tularemia culture from water voles. K. A. Doro-feev (1937 - 1941) described in detail tularemia in farm and industrial animals and proposed to isolate the causative agent of this disease in independent genus Francisella. Tularemia is widespread in the United States and many countries in Europe and Africa. The disease is recorded mainly in steppe areas during years of increased rodent reproduction, as well as in the valleys of large rivers, where water bee-eater, as an object of industrial hunting, often infects people. Economic losses from tularemia are insignificant due to the benign course of the infection in most farm animals.

The causative agent of the disease- Francisella tularensis from the genus Francisella Dorofeev is a very small (0.3...0.7) x (0.2...0.6) µm, immobile polymorphic gram-negative bacterium, which often takes on a coco-shaped form. It has a delicate capsule and does not form spores. Painted with all aniline dyes, as well as Romanovsky - Giemsa with long exposure (1-1.5 hours). Francisels are cultivated only on selective nutrient media - McCoy, Francis, meat-peptone agar with cystine and blood, and egg-yolk medium. The growth of the microbe is detected 2-7 times after inoculation of the pathological material, observed in the form of moist, shiny, low-grained mucous droplets.

The causative agent of tularemia is pathogenic for guinea pigs and white mice. Chicken embryos die within 72 - 120 hours after infection. A characteristic feature of Francisel is the ability to remain in natural conditions for a long time. They remain in water for 90 pores, in hay and straw haystacks - 3 months, in grain - 133 pores, in soil - 75 pores, in the skins of rodents - 45 pores, in dried rodent corpses - up to 90 pores, in frozen meat - up to 93 pores, in frozen milk - up to 104 pores, in the body of pasture ticks - up to 240 pores, salted skins - up to 15 pores. Quickly inactivated by exposure high temperatures: at 100 °C - instantly, at 60 °C - after 5-10 minutes, in sunny conditions after 20-30 minutes. Conventional disinfectants in accepted concentrations quickly neutralize the causative agent of tularemia.

Epizootologydiseases. Under natural conditions, wild rodents are susceptible to tularemia - hares, rabbits, field mice, field beetles, muskrats, beavers, gophers, which create permanent natural infection cells. Farm animals are insensitive to the causative agent of tularemia, with the exception of lambs and piglets. Sporadic cases of the disease have been described in sheep, pigs, horses, cows, as well as in dogs, chickens and wild birds.

The source of the causative agent of the disease for domestic animals is sick, recovered and dead rodents, which contaminate pastures, watering places, and fodder with Francisella. Infection in natural cells occurs due to grazing of animals in contaminated areas or drinking from unfavorable water bodies. The causative agent of the disease can be carried by stinging insects and ticks.

Outbreaks of the disease in native animals are observed mainly in the spring-summer-autumn seasons, which is associated with the significant migratory activity of rodents and the availability of a transmission route for the transmission of the pathogen. Tularemia in native animals occurs in the form of sporadic cases or small enzootics and is determined by the number of heads that end up in the natural cell of wild rodents. Spring epidemics among people are associated with the procurement of industrial rodent skins; autumn and winter epidemics are associated with delayed threshing of bread and the migration of infected rodents near human habitation.

Pathogenesis Not studied enough. From the site of penetration, the pathogen spreads throughout the body through hematogenous and lymphogenous routes and multiplies. The disease develops according to the type of bacteremia, with damage to the vascular, lymphatic and nervous systems, the formation of necrosis in the lungs, liver, spleen, and brain. Pregnant animals may develop metritis with subsequent infection of the fetus.

Clinical signs and course of the disease. In adult animals the infection was asymptomatic, in young animals it was acute. U Lambs At the onset of the disease, fever (40.5-41 °C), accelerated pulse and breathing are observed, sick animals lag behind the flock and stand with their heads bowed. After 2-3 pores, the temperature decreases, signs of damage to the central nervous system develop - convulsions, paresis and paralysis of the posterior ends. The mucous membranes are anemic, the retropharyngeal, cervical and prescapular lymph nodes are enlarged. Sometimes tularemia is accompanied by signs of catarrhal conjunctivitis, rhinitis, profuse diarrhea and severe exhaustion. Sick lambs for the most part die in the first 3-7 years of the disease.

U Cattle The disease has become latent; lethality is detected only during serological studies. Sometimes there is an increase in superficial lymph nodes, mastitis, and paralysis of the hind limbs. U Pigs The disease manifests itself only in young people. Fever, depression, loss of appetite, and cough are observed among weaned piglets. U Horses Latent diseases have escaped, sometimes abortions occur. U Rabbits The disease is accompanied by signs of rhinitis, the formation of abscesses in the subcutaneous lymph nodes. U Kotov Severe exhaustion, lack of appetite, congestion, vomiting, and indigestion are observed. In fur animals If tularemia is malignant, the mortality rate can reach 50%. Pathological changes Not typical. The corpses of animals are emaciated; abscesses sometimes appear in enlarged lymph nodes. Small cells of necrosis and hemorrhage are observed in the liver, lungs, and spleen. Almost all dead animals show signs of septicemia.

Diagnosis It is based on epizootic and epidemiological data (the presence of an epizootic among rat-like rodents, disease in humans), as well as on the results of laboratory studies of pathological material from sick and dead animals. To diagnose sheep, allergy tests are carried out.

Laboratory diagnostics. For lifetime diagnosis, bacteriological studies are carried out on the blood of sick animals, which is taken during the period of increased body temperature, and punctures from the affected lymph nodes. When cutting corpses, blood and pieces are taken internal organs and lymph nodes. It should be noted that the isolation of a culture of the causative agent of tularemia is associated with significant difficulty due to the high requirements of Francisel for nutrient media. A more accurate method for identifying tularemia bacteria is a bioassay on white mice, which, after parenteral administration of infected pathological material, die after 3-4 pores, or guinea pigs, the death of which occurs 4-6 pores after infection. Serological studies involve conducting RA with blood serum collected at 8-13 days from the onset of the disease. Serological studies make it possible not only to diagnose the septic form of infection, but also to establish the latent course of tularemia. For allergic diagnosis of tularemia in sheep, tularin is used, which is injected subcutaneously into the sub-tail fold in a dose of 0.3 ml. The results of the reaction are taken into account 24 and 48 hours after administration of the drug. Positive allergic reaction They consider the formation of an incendiary painful dough-like swelling at the site of injection of tularin and an increase in the thickness of the skin fold.

Differential diagnosis. Provides for the need to exclude diseases such as paratuberculosis, brucellosis, anaplasmosis and coccidiosis. For this purpose, epizootological, clinical and pathological data are used, as well as the results of bacteriological and serological studies.

Treatment. Funds specific therapy for tularemia has not been developed. Antibiotics are used for treatment wide range actions, the best after previous identification of the sensitivity of the pathogen to them. Combination antibiotic therapy with sulfa drugs and symptomatic treatment. If necessary, resort to surgical removal affected lymph nodes.

Immunity. After testing for tularemia, animals develop long-lasting, stable immunity. No vaccine has been proposed for the specific prevention of tularemia in animals. In endemic cells, a live protitularemia vaccine is used to vaccinate people (B. Ya. Elbert, N. A. Raisky, 1946).

Tularemia in humans. Occurs as a result of careless handling during the removal and processing of the skin of sick industrial animals, threshing of stacks inhabited by infected rodents, consumption of water and food that are contaminated with secretions of infected animals. Laboratory workers can become infected while cutting up cadavers and handling pathogen cultures. Infection occurs through the skin, mucous membranes of the respiratory tract, and tonsils. The incubation period lasts 10-12 years. Patients experience fever, headache, pain in the legs and back. In the case of the glandular form of the disease, there is soreness and enlargement of the lymph nodes with suppuration and the formation of ulcers, the typhoid form - fever for 7-10 years, intoxication of the body, enlargement of the liver and spleen, decreased ability to work, which is restored very slowly. For the purpose of personal prevention diagnostic studies pathological material suspicious for tularemia should be carried out wearing a respirator mask, using rubber gloves and safety glasses. Before cutting, animal corpses should be disinfected with a % solution of carbolic acid or Lysol.

Pathogen: Francisella tularensis discovered in 1912. McCoy and Sh. Chepin in the Tulare area. Tularemia bacteria are very small coccoid and rod-shaped, non-spore-forming, non-motile cells, G~. Bacteria are characterized by polymorphism. They can have the shape of weights, very small cocci; aerobic, does not grow on ordinary nutrient media, develops well at 37°C in media rich in vitamins, for example, in yolk medium.

The pathogen remains viable in water for 3 months, in meat for 93 days, and in milk for 104 days. Sun rays kill in 30 minutes, heating at 60°C - in 5-10 minutes.

Epizootology. Course and symptoms. Mostly rodents are affected. Humans are very sensitive to tularemia. Farm animals are little sensitive to the causative agent of tularemia; they become infected in natural foci. Sporadic cases have been reported in sheep, cattle, horses, pigs, reindeer, camels, cats, and poultry.

Young animals are more susceptible. Infection occurs nutritionally, by airborne droplets and as a result of the bites of arthropod insects - ticks, fleas, mosquitoes, horseflies. The vector-borne route of infection determines the spring-summer-autumn seasonality of the disease; the preservation of the pathogen in the external environment is facilitated by long-term carriage of bacteria various types mammals and arthropods.

Incubation period: 4-12 days. In cattle, enlarged lymph nodes, mastitis, abortions, in some cases can occur in the form of paralysis with fatal. Pigs, camels, and buffaloes experience loss of appetite, chills, cough, rapid breathing, enlarged subcutaneous lymph nodes, and sweating in piglets. In lambs, depression, fever, increased pulse and respiration, pallor of the mucous membranes, and then paresis and rigidity of the muscles of the limbs are noted. In horses, along with clinical expressed form(abortion for 4-5 months), lung and asymptomatic, detected by the agglutination reaction.

Pathological and anatomical changes. Sheep killed in acute stage diseases, find changes in inside skin in places of tick bites, translucent areas the size of a pea appear there, sometimes with slight hemorrhage and tissue compaction, skin ulcerations and necrotic areas are also observed, especially in the axillary region. Subcutaneous tissue hyperemic, nodules are noted in it, often undergoing disintegration. At chronic form diseased sheep are exhausted. Nodules such as infectious granulomas are observed in the lungs, liver, spleen, serous fibrinous pleurisy or pneumonia without pleurisy, a strong venous stasis with injection of blood vessels on the inside of the skin, as well as in the lungs, liver, spleen and intestines. The heart is filled with dark, weakly coagulated blood, the cardiac muscle is flabby, and pinpoint hemorrhages are common under the epicardium. In pigs, mainly in piglets, signs of pleuropneumonia are found, in some cases purulent processes in the submandibular and parotid lymph nodes.

Diagnostics. A punctate from enlarged lymph nodes, from an aborted fetus or the entire fetus, urine, and feces is sent to the laboratory. After death - liver, kidneys, spleen, enlarged lymph nodes from large animals, rodent corpses.

Conduct smear microscopy, bacteriological and serological studies, allergy diagnostics, bioassay.

Differential diagnosis. In sheep, tularemia should be differentiated from listeriosis and other diseases associated with paralysis of the limbs and comatose state, in piglets - from hemorrhagic septicemia.

Prevention and treatment. Treatment: antibiotics are prescribed (gentamicin, tetracycline), a vaccine made from killed tularemia bacteria.

Prevention: consists of carrying out general anti-epidemic measures in outbreaks and immunizing people. Specific prevention is carried out with the live GaiskyElbert vaccine, as well as inactivated vaccine prepared from a protective antigen. The vaccine is produced in dry form. Apply cutaneously once. The duration of post-vaccination immunity is 3-6 years.

Veterinary and sanitary examination. Sick animals are not allowed to be slaughtered. In case of slaughter, all products must be destroyed. Products that have come into contact with carcasses, organs or blood of animals with tularemia are boiled. The premises where carcasses or organs from sick animals were located are disinfected with a hot 2% solution of caustic soda. The working tool is boiled in a 5% soda ash solution for 30 minutes. Contaminated gowns and other protective clothing are sterilized in autoclaves at 1.5 atm - 20 minutes.

Back in the days Cold War biologists in the USSR and the USA calculated that the effect of spraying this agent over the cities of a potential enemy would be such that even nuclear weapons would not be needed. So this disease is extremely dangerous, and you need to know as much as possible about it.

The disease is caused by the bacterium Francisella tularensis. This organism can form spores and belongs to the category of gram-negative microorganisms. Interestingly, Francisella tularensis accounts for " distant relative"causative agent.

The taxonomic status of Francisella has been revised for last decades. Thus, in the recent past, the subspecies F. tularensis tularensis was discovered, disease-causing type "A", F. tularensis holarctica, which causes tularemia type "B". There is also a subspecies of F. novicida, which causes, accordingly, type “C” disease.

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This strain has weak virulence and is almost not widespread. The most “poisonous” class is “A”, predominantly distributed in North America. Even with timely treatment, mortality can reach 30%. Type "B" is not so dangerous. It is the cause of more than 90% of tularemia cases in our country and adjacent countries.

Epidemiology and transmission

The disease is most common in sheep, but Tularemia in cats and dogs is also quite possible. Cats are exposed increased risk because of tendency to hunt mouse-like rodents. Also latest research prove that they are the ones with increased susceptibility. One of the most typical natural hosts of F. tularensis tularensis are rabbits, and for F. tularensis holarctica a suitable “substrate” is gophers.

Natural foci of infection exist in North America and Eurasia. So, on the territory of the former Soviet Union Some territories of Northern Kazakhstan and Kyrgyzstan can be considered such a focus. The pathogen is often found in the Orenburg region, where tularemia is relatively regularly recorded in dogs and sheep.

Tularemia can be transmitted by airborne droplets, direct contact promotes transmission; infection also occurs through direct ingestion of the pathogen (water with amoebas), when bitten by ticks or infected animals. Airborne transmission is the most dangerous, as it develops pulmonary form infections.

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Unfortunately, very cases are often recorded infection of humans through contact with sick pets. At the slightest suspicion of tularemia, you must immediately isolate the animal and urgently contact both doctors and a veterinarian!

Clinical picture of the disease

What are the symptoms of this infection? The incubation period is 1–10 days. The pathogen develops most quickly in the body of cats. Clinical manifestations depend both on the specific type of pathogen and on the routes of its introduction into the body. For domestic animals, bacteremia is most common, accompanied by fever and respiratory tract infection.

Also in cats a common symptom pathology is swelling and soreness of the regional pharyngeal lymph nodes. The heart rate rises sharply and breathing movements, appears