Dangerous pneumonia in dogs: how not to confuse it with a cold and provide timely assistance. Pneumonia in animals

In large livestock farms and industrial complexes, especially if veterinary and sanitary rules for keeping animals are violated, the disease can become widespread and the number of sick people can reach 30-50. Clinical and anatomical forms of pneumonia Pneumonia is divided into lobular limited lobular, which includes bronchopneumonia catarrhal pneumonia purulent metastatic characterized by involvement in the pathological process in the form of small foci of individual lobes of the lungs or all lungs and an abscess...

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1. Bronchopneumonia (catarrhal pneumonia) Bronchopneumonia - - - 3
2. Clinical and anatomical forms of pneumonia - - - - - - - - - - - - - - - - - - - - - -4
3. Etiology of catarrhal bronchopneumonia - - - - - - - - - - - - - - - - - - - - - - - 9
4. Pathogenesis of catarrhal bronchopneumonia - - - - - - - - - - - - - - - - - - 10
5. Symptoms of catarrhal bronchopneumonia - - - - - - - - - - - - - - - - - - -12
6. Pathomorphological changes in catarrhal bronchopneumonia - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -13
7. Diagnosis and differential diagnosis of catarrhal bronchopneumonia - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - 15
8. List of used literature - - - - - - - - - - - - - - - - - - - - - - 17

Analysis of a diagnosed case of disease

1. Bronchopneumonia (catarrhal pneumonia) Bronchopneumonia

The disease is characterized by inflammation of the bronchi and alveoli, accompanied by the formation of catarrhal (mucous) exudate and filling the bronchi and alveoli with it. The pathological process has a lobular (focal) character. Initially, the bronchi and lobules of the lung are affected, after which inflammation can cover several lobules, segments and even lobes of the lungs, as a result of which the disease will be characterized as small-focal, large-focal or confluent pneumonia.

Bronchopneumonia is widespread among animals of all species, in all geographical areas, and especially in young animals during the periods of weaning, growing, and fattening. In large livestock farms and industrial complexes, especially if veterinary and sanitary rules for keeping animals are violated, the disease can become widespread, and the number of cases can reach 30-50%.

The diagnosis of catarrhal bronchopneumonia was made based on medical history, etiological factors, clinical picture and the results of the pathological autopsy.

2. Clinical and anatomical forms of pneumonia

Pneumonia is divided into lobular (limited, lobular), which include bronchopneumonia (catarrhal pneumonia), purulent (metastatic, characterized by involvement in the pathological process in the form of small foci of individual lobes of the lungs, or all lungs and lung abscess), hypostatic (congestive), mycotic (fungal), putrefactive (lung gangrene), atelectatic, aspiration, silicic (when the lungs are dusted with silicon dust), anthracose (when the lungs are dusted with coal dust), gasoline and some others, and lobar (spilled), which include croupous (fibrinous) pneumonia, contagious pleuropneumonia of horses, widespread pneumonia of large cattle etc. However, the most common are bronchopneumonia, accounting for more than 60% of all pulmonary diseases, as well as purulent, hypostatic, mycotic, putrefactive and lobar pneumonia.

Exudative pneumoniaIt can be serous, catarrhal, fibrinous, purulent, hemorrhagic, ichorous and mixed.

Serous pneumoniabegins with exudation, which is expressed by inflammatory hyperemia, the phenomenon of serous exudation, when sweat begins to flow from the walls of the capillaries into the lumen of the alveoli serous exudate(inflammatory edema). Macroscopically tissuelightly compacted, red or pink in color, the pleura is smooth, slightly cloudy (opalescent) flows from its surface and liquid Under microscopy, the alveoli are filled with a turbid fluid, pink-stained with eosin, with individual leukocytes and desquamated respiratory epithelial cells. Serous pneumonia is often the initial process of a number of other pneumonias, which later develop into lobar or catarrhal bronchopneumonia.

Fibrinous (lobar) pneumoniasevere pneumonia in farm animals. It is characterized by the sweating of fibrinous exudate into the lumen of the alveoli, which, upon leaving the lumen of the vessels, turns into dead fibrin protein. The process takes place in several stages:
1) stage of hyperemia: serous exudate flows into the lumen of the alveoli from the capillaries. The affected areas of the lung are bluish-red in color, soft in consistency, and juicy when cut;

2) stage of red hepatization - fibrinogen-rich exudate containing leukocytes and erythrocytes flows from the vessels into the lumen of the alveoli. The affected areas of the lung filled with such exudate acquire a dark red color (hemolysis of red blood cells) and a dense consistency similar to the consistency of the liver red hepatization;

3) stage of gray hepatization areas of the lung acquire a gray tint, since leukocytes that have undergone dystrophic changes. The exudate accumulated in a large volume in the affected areas compresses the lung tissue, and the blood vessels also collapse;

4) resolution stage: leukocyte enzymes dissolve fibrin protein in the lumen of the alveoli and interstitial tissue. The lung tissue turns dark red or grey colour, becomes a dense consistency, the pieces sink in the water. When cut, a reddish liquid flows from the surface of the dark red areas.

The non-simultaneous development of stages in different lobules of the lung gives the inflamed areas a marble pattern specific to this type of inflammation. The resemblance to a marble pattern is enhanced by severe swelling of the interlobular septa, which in the form of grayish gelatinous stripes are especially pronounced in the lungs of cattle and pigs.

Histologically, in the stages of hyperemia and red hepatization, the alveoli are filled with exudate with fibrin threads, erythrocytes and leukocytes, the alveolar septa are dilated, and the capillaries are filled with blood. In the stage of gray hepatization, there are almost no red blood cells in the exudate, a lot of fibrin and leukocytes, the lumen of the capillaries is narrowed. In the interlobular connective tissue, a proliferation of reticulohistiocytic cells and fibroblasts is observed, most pronounced in the resolution stage. Even with a favorable outcome of inflammation, changes remain in the lungs, which are defined as induration and are characterized by thickening of the connective tissue, often with hyaline degeneration. The latter becomes homogeneous, with a small number of elongated nuclei.

The outcome of lobar pneumonia depends on the degree of filling of the alveoli and the associated circulatory disorders. Yellow hepatization may occur with the cleansing of the alveoli from fibrin and restoration of their function or carnification (from the Latin sago - meat, fictio formation), characterized by the germination of fibrin by connective tissue and blood vessels, as a result of which pneumonic areas resemble meat in color and consistency. This is observed when fibrin resorption is delayed, when the affected areas of the lungs, overgrown with connective tissue, cannot return to their normal state. The outcome is the form of sequestration (from lat. sequestro separate) is associated with necrosis of inflamed areas, their separation from the surrounding tissue. This occurs in severe cases of lobar pneumonia, when fibrin accumulates in the alveoli in such quantities that blood circulation in them stops, and the lymphatic vessels often undergo thrombosis. Melting of the dead section of the lung occurs at its border with living tissue, and a connective tissue capsule often develops here. Upon opening, the sequester can be completely removed and the anatomical structures of the lung can be distinguished in it. The outcome of sequestration is sometimes observed in cattle with widespread pneumonia.

Thus, the pathological signs of lobar pneumonia are: extensive (lobar) lesions, hepatization (compaction) of the lung to the consistency of liver (hepatization), a dryish, granular cut surface.

Purulent inflammationis expressed by the formation of abscesses of varying sizes in the lungs (abscess pneumonia) or catarrhal-purulent diffuse inflammation. Abscesses in the lungs can form independently or as a complication of one or another inflammation. They come in different sizes and consist of accumulations of purulent bodies, colonies of pyogenic microorganisms and neutrophilic leukocytes in varying degrees degeneration. Often abscesses are also enclosed in a capsule, which consists of an inner (pyogenic) and outer (fibrous connective tissue) layer.

Catarrhal-purulent (mixed) inflammationmay begin with acute catarrhal bronchopneumonia and progress as a complication to purulent pneumonia. The accumulated leukocytes eventually undergo degenerative changes and turn into purulent bodies. Exudate rich in protein and cellular elements accumulates in the alveoli.

Hemorrhagic pneumoniacharacterized by a predominance in exudate large quantity red blood cells Observed in a number of infectious diseases (anthrax, swine fever), which occur with a violation of the integrity of the walls blood vessels and death of red blood cells. The intervening connective tissue is saturated with red blood cells and becomes dark red in color. Histologically, a mass of red blood cells is observed in the alveoli.

Ichorous (putrefactive) inflammationmay be a complication of fibrinous inflammation with tissue necrosis. Putrefactive microbes begin to multiply in the dead tissue, and part of the tissue melts to form cavities with jagged, corroded edges.

Necrotizing (alterative) pneumoniaobserved in most animals with necrobacteriosis as a metastatic process of transfer of microbes to the lungs from infected wounds. In addition, necrotizing pneumonia can be the result of a complication when toxic substances enter the respiratory tract or foreign bodies(aspiration pneumonia), and medical error, improper administration of medications. Initially, necrotizing pneumonia develops as serous-fibrinous inflammation, but the inflamed areas quickly undergo necrosis and only zones of serous-fibrinous inflammation remain around them. With necrotic inflammation, the lung is compacted, the surface is unevenly colored, and the pleura is rough. On a section, the lung tissue looks like foci of light gray or pale pink color. Histologically, at the border between dead and living tissue, a demarcation shaft is visible, consisting of an accumulation of leukocytes and histocytes.

The outcome of such pneumonia is usually fatal, and in best cases small necrotic areas are encapsulated.

Productive pneumoniamore often observed as an outcome of catarrhal bronchopneumonia in diseases such as glanders and tuberculosis. In this case, the exudation processes almost stop, and proliferation becomes predominant. The cell proliferation consists of respiratory epithelium, lymphocytes and leukocytes. The lung has a dense consistency, is difficult to cut, its surface is lumpy, light gray or light pink in color.

3. Etiology of catarrhal bronchopneumonia

Bronchopneumonia is mostly secondary disease accompanying other diseases. It has a polyetiological basis and arises as a result of complex effects on the body of various kinds. unfavorable factors, in particular, weakening immune status animals as a result stress state, hypothermia, overheating, inhalation of polluted air, malnutrition etc. The disease usually accompanies canine distemper, hemorrhagic septicemia of sheep, foot and mouth disease, tuberculosis, helminthiasis, etc.

It is also believed that a significant role in the occurrence of bronchopneumonia against the background of the above causative factors is initially played byopportunistic, a viral and bacterial infection that is constantly present in the respiratory tract or enters them, and the viral factor is the trigger (initial), and the microbial factor that arises against this background continues and intensifies the pathological process, in many cases determining, and often completing in a negative way.

Of the viruses, these are most often influenza viruses, parainfluenza, rhinotracheitis, adenoviruses, enteroviruses, etc., and of bacterial flora pneumococci, staphylococci, streptococci, proteus, as well as mycoplasmas and fungi are usually isolated.

The reasons may also be the entry of foreign particles and feed into the alveoli, often leading to the development of special catarrh lungs, called aspiration pneumonia. The disease sometimes occurs as a result of the development of the process of laryngotracheitis.

4. Pathogenesis of catarrhal bronchopneumonia

Bronchopneumonia is considered as general disease, manifested by a violation of all systems and functions of the body, but with localization of the process in the lungs.

Under the influence of etiological factors, the functioning of the bronchi and alveoli occurs. In the submucosal layer of the bronchial membrane, a spasm initially occurs, and then paresis of the capillaries and against this background, stagnation of blood, as a result of which swelling and hemorrhages occur in the lung tissue.

In the initial stages of the disease, this is accompanied by catarrhal or serous-catarrhal inflammation. As a result, non-coagulable exudate, consisting of mucin, leukocytes, erythrocytes, bronchial epithelial cells and microflora, enters the lumen of the bronchi and alveoli. Subsequently, the organization of exudate, carnification of the lung tissue, induration, calcification of the resulting pneumonic foci and disintegration of the bronchi and lung tissue occur.

In the acute course of the disease, the superficial lobules of the lungs are primarily affected. Interlobular connective tissue is a barrier to the transition of inflammation from the affected lobules to healthy ones, although in the future this function may be lost.

At chronic course the process can transform into lobar due to the merging of individual foci of inflammation into large areas and represent confluent (lobar) pneumonia (Fig. 1). Complications (more often in pigs) can be in the form of adhesive pleurisy and pericarditis, as well as pulmonary emphysema.

As a result of the absorption of toxins and decay products of dead tissue from foci of inflammation into the lymph and blood, intoxication of the body can occur, usually accompanied by varying degrees of increase in body temperature (remitting fever), disruption of the functioning of the cardiovascular, respiratory, digestive, nervous and other systems of the body.

Thus, the quantitative and qualitative indicators of erythropoiesis change. In particular, there is a delay in the maturation of red blood cells, the population of old cells increases, and the hemoglobin content in one red blood cell decreases. To varying degrees, but more often consumption is reduced by 2-3 timesoxygen per unit mass of the animal, and the degree of saturation of arterial blood with oxygen decreases to 70-80% instead of 97-98%, resulting in a disorder of tissue gas exchange. Disorders of the digestive and nervous systems are accompanied by decreased appetite and dystonia of the gastrointestinal tract, general weakness, decreased performance and productivity of animals.

Rice. 1. Lobar catarrhal bronchopneumonia in a calf

5. Symptoms of catarrhal bronchopneumonia

Sick animals exhibit depression, weakness, loss or decreased appetite, and an increase in general body temperature by 1-2 0 C (may not be present in old and emaciated animals), cough, nasal discharge, hard breathing, mixed shortness of breath, initially dry, and after 2-3 days moist rales in the lungs. Percussion establishes limited areas of dullness, bordering areas of normal pulmonary percussion sound and found mainly in the area of ​​the apical and cardiac lobes of the lungs. With deeply located foci of inflammation, there may be no changes in percussion sound.

In the confluent form of the disease, auscultation and percussion data are similar to those found in lobar pneumonia in the stage of hepatization. As a rule, there is tachycardia and increased second tone.

The manifestation of the disease largely depends on the age and type of animal. Thus, in horses and sheep it is characterized by a relatively rapid spread pathological process in the lungs compared to that observed in pigs and cattle. In young and old animals, bronchopneumonia is usually more severe. The disease often accompanies: disorders of the cardiovascular, digestive and nervous systems, as well as kidneys, liver and other organs with their characteristic manifestations.

6. Pathomorphological changes in catarrhal bronchopneumonia

Upon opening chest the most characteristic changes are found in the lungs and bronchi. The lungs are incompletely collapsed and usually dark red with a grayish-bluish tint. There may be hemorrhages in their parenchyma and under the pleura. In affected areas they are compacted, airless and protrude above neighboring areas. Their cut surface is smooth, and when pressure is applied to it, a bloody or grayish liquid flows out. The interstitial tissue of the affected part of the lungs is dilated, saturated with serous exudate, gelatinous. In the center of the inflammatory foci are visible. lumens of the bronchi, often filled with exudate. Wedge-shaped atelectatic (collapsed) foci of meat-like consistency are always found. Near the affected areas, vicarious (compensatory) emphysema almost always occurs, and in cattle, interstitial emphysema. There may also be purulent or cheesy lesions of varying sizes.

Microscopy reveals dilations of the capillaries of the pulmonary septa, protruding into the lumen of the alveoli, which contain serous exudate with a significant amount of exfoliated epithelial cells, leukocytes, erythrocytes and microbes (Fig. 2). With bronchopneumonia of aspiration origin, there may be purulent or gangrenous areas.

In chronic catarrhal bronchopneumonia, the lung is dense, fleshy, the consistency resembles a gland (splenization), often lumpy on the surface, and granular in section (Fig. 3).

Dry or exudative pleurisy is often detected, as well as an increase in bronchial lymph nodes. From nonspecific changesat chronic form diseases include exhaustion, dystrophy of the myocardium, liver, kidneys, and muscle atrophy.

Rice. 2. Catarrhal bronchopneumonia

a bronchus, b alveoli filled with exudate

Rice. 3. Chronic catarrhal bronchopneumonia of cattle

7. Diagnosis and differential diagnosis of catarrhal bronchopneumonia

Based on the above clinical symptoms taking into account the medical history, etiological factors and relevant special methods studies, as well as the results of a pathological autopsy, the diagnosis is not difficult to make.

Hematological research methods establish the presence of neutrophilic leukocytosis with a shift to the left, lymphopenia, eosinopenia, monocytosis, accelerated ESR, a decrease in reserve alkalinity, a decrease in catalase activity of erythrocytes, a drop in the level of oxygen saturation of hemoglobin in arterial blood.

However, the most objective and most precise method X-ray examination is used to diagnose the disease. With it, in the initial stages of the disease, homogeneous lesions with uneven contours are easily detected in the apical and cardiac lobes. In patients with chronic confluent (diffuse) forms of bronchopneumonia, radiographic examination reveals diffuse, extensive, densely shaded areas of the lungs. In this case, the border of the heart and the contours of the ribs in the affected areas do not differ. For the mass diagnosis of bronchopneumonia in calves, sheep, pigs in general and especially on large livestock farms, R. G. Mustakimov proposed a fluorographic method.

In particular necessary cases To establish and clarify the diagnosis, a biopsy from the affected areas of the lungs, bronchography, bronchophotography, examination of tracheal mucus, nasal discharge, and other research methods are used.

In differential diagnostic terms, bronchitis, other pneumonias, especially lobar pneumonia, as well as infectious and invasive diseases accompanied by lesions should be excluded respiratory tract and lungs, in particular, contagious pleuropneumonia, diplococcal infection, pasteurellosis, salmonellosis, mycoses, mycoplasmosis, respiratory viral infections, dictyocaulosis, metastrongylosis, ascariasis, etc.

With bronchitis, there is no or only minor (by 0.5-1 With C) an increase in general body temperature, there are no areas of dullness in the lungs, and an x-ray examination reveals only an increase in the pattern of the bronchial tree and the absence of areas of shading in the lungs. At autopsy, the mucous membrane is hyperemic, swollen, there is exudate in the lumen of the bronchi, destroyed bronchial epithelium, loss of villi in the cells. The exudate contains a large number of dead cells, leukocytes, erythrocytes, and microbes. The mucous membrane of the bronchi is often atrophied, their lumen is narrowed, sometimes expanded, there is mucous exudate in the lumen of the bronchi, and emphysema in the marginal areas of the lungs. With purulent and fibrinous bronchitis, the mediastinal lymph nodes are enlarged and swollen.

Lobar pneumonia is excluded by its characteristic suddenness of onset, staged course, constant type of fever, lobar focality, fibrinous discharge from the nose.

Pathoanatomical signs of lobar pneumonia are: extensive (lobar) lesions, hepatization (compaction) of the lung to the consistency of liver (hepatization), dryish, granular cut surface.

Other pneumonias are excluded based on their characteristic symptoms and using special research methods.

To differentiate from infectious diseases that have a similar pathomorphological picture, the pathological material should be sent to the laboratory.

8. List of used literature:

1. Internal diseases of animals / Under general. Edited by G.G. Shcherbakova, A.V. Korobova. St. Petersburg: Lan Publishing House, 2002. 736 p.

2. Autopsy and pathological diagnosis of agricultural diseases. animals / A.V. Zharov, I.V. Ivanov, A.P. Strelnikov, etc. M.: Kolos, 1982.

3. Kokurichev P. I., Domann B. G., Kokuricheva M. P. Pathological anatomy agricultural animals. Atlas. St. Petersburg: Agropromizdat, 1994.

4. Pathological diagnosis of cattle diseases / A.V. Akulov, V.M. Apatenko, N.I. Arkhipov, etc.; Ed. V.P.Shishkova, A.V.Zharova, N.A. Naletova. M.: Kolos, 1987.

5. Workshop on pathological anatomy of agriculture. animals/A. V. Zharov, I. V. Ivanov, A. P. Strelnikov, etc. M.: Agropromizdat, 1989.

6. Strukov A. I., Serov V. V. Pathological anatomy. M,: Medicine, 1993.

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Lobar pneumonia
(Pneumonia crouposa) is a disease characterized by fibrinous inflammation involving the lobes of the lung and the stages of the pathological process. Mostly horses and sheep are affected. In specialized fattening farms cattle and raising heifers, pneumonia is more often observed among calves 1-3 months of age.

Etiology. In the occurrence of lobar pneumonia, paramount importance is given to two leading factors: pathogenic microflora and allergic condition body. When examining sputum and material from affected areas of the lungs, pneumococci, staphylococci, diplococci, streptococci and other microorganisms are isolated. However, the listed types of microbes can also be found in the tracheal mucus of healthy animals.

Most researchers have recently considered lobar pneumonia as one of the types of allergic reactions of the body that occurs under the influence of a strong irritant. This condition can develop after sudden hypothermia of a hot horse, driving sheep in hot weather through cold mountain rivers, or quick translation cattle from warm premises to cold and damp ones.

Pathogenesis.
The development of the pathological process in lobar pneumonia occurs quickly (hyperergic inflammation) and is characterized by its coverage of large areas of the lungs within several hours and the exudation of hemorrhagic-fibrinous exudate into the cavity of the alveoli. As a rule, the cranial, ventral and central parts of the lung are affected sequentially, and in some cases the caudal and dorsal parts are also involved in the pathological process. Spreading inflammatory process in the lungs occurs hematogenously or through the lymphatic tract.

In the typical course of lobar pneumonia, if the initial period of the disease is not treated with antibiotics or sulfonamide drugs, a certain staged development of the inflammatory process is characteristic. There are four successive stages.

The stage of inflammatory hyperemia, or hot flash, lasts from several hours to 2 days. At this stage, there is a pronounced overflow of blood into the pulmonary capillaries, swelling of the alveolar epithelium and exudation of serous-hemorrhagic exudate into the lumen of the alveoli.

The stage of red hepatization is characterized by an increase in the amount of coagulating exudate in the alveoli up to the complete displacement of air from the alveoli; the exudate contains a large number of leukocytes and fibrin. The duration of the stage is 2-3 days.

The stage of gray hepatization lasts 2-3, sometimes up to 4-5 days. At this stage there are fatty degeneration fibrinous exudate and a further increase in the number of leukocytes in it.

The resolution stage is characterized by liquefaction of fibrinous exudate under the action of proteolytic and lipolytic enzymes, its resorption and partial release through the respiratory tract during coughing. The alveoli fill with air, which leads to the restoration of pulmonary gas exchange. The duration of the resolution stage ranges from 2-5 days.

In lobar pneumonia, as a result of exclusion of large areas of lung tissue from gas exchange and intoxication with inflammatory products and microbial toxins, the functions of the central nervous system, heart, liver, kidneys, intestines and other organs are disrupted. At severe forms course of the disease, if vigorous treatment is not carried out, death occurs against the background of progressive asphyxia from paralysis of the respiratory center or cardiovascular failure.

Pathological changes are localized in the lung tissue and are characterized by the stages of the pathological process. In the stage of inflammatory hyperemia, the affected areas of the lungs are enlarged in volume, swollen, red-blue in color, and do not sink in water - on the cut, a foamy reddish liquid is released from the lumen of the bronchi when pressed.

In the stages of red and gray hepatization, the affected lungs are airless, dense to the touch, resemble liver in consistency (hence the name “hepatization”), and drown in water. In the stage of red hepatization, coagulated fibrinous exudate gives the lungs a red color, and in the stage of gray hepatization, the lung has a grayish or yellowish color due to fatty degeneration or migration of leukocytes. In the resolution stage, the lung resembles the spleen in consistency and color.

In other organs with lobar pneumonia, nonspecific changes of varying degrees can be detected: degenerative-inflammatory changes in the myocardium, liver, intestines, kidneys, overflow of the meninges with blood, swelling and an increase in the volume of mediastinal lymph nodes, etc.

Symptoms. The course of lobar pneumonia is acute. The disease occurs suddenly, without warning, in horses, often during work or training.

A rapidly increasing general depression, loss of appetite, hyperemia and yellowness of the mucous membranes, rapid and intense breathing are noted. The typical development of lobar pneumonia is characterized by a constant type of fever: from the first day of the disease until the resolution stage, the temperature constantly, regardless of the time of day, remains at 41-42 °C. The pulse is increased against the norm by 10-20 per minute, the heartbeat is pounding, the second heart sound is increased.

Symptoms of damage to the respiratory system are determined by the stages of development of the inflammatory process in the lungs. In the first days of the disease, a dry, painful cough is noted, which in subsequent days is replaced by a dull and wet cough. In the stage of red hepatization in horses, rusty or brown fibrinous exudate can be observed flowing from the nasal openings; this outflow can be one-sided or two-sided.

Upon auscultation in the stages of inflammatory hyperemia and resolution, harsh vesicular or bronchial breathing, crepitus, and moist fine or coarse bubble rales are detected. In the stages of red and gray hepatization, dry rales are heard, bronchial breathing or breath sounds are absent in the areas of lung damage.

Percussion in the stages of inflammatory hyperemia and resolution reveals tympanic or tympanic sounds over the affected lungs, and in the stages of red and gray hepatization - large areas of dullness with a characteristic arched, convex upward dullness border located in the upper third of the pulmonary field (Fig. 27). As the exudate resolves and the animal recovers, the dull percussion sound is replaced by a dull, then tympanic and normal pulmonary sound.

If the course of the disease is favorable, with the onset of the resolution stage, which usually happens on the 7-8th day from the moment of illness, improvement occurs general condition animal, lowering body temperature, normalizing the respiratory and cardiovascular systems.

If, from the first days of the disease, vigorous treatment is carried out using antibacterial drugs, lobar pneumonia takes on an atypical form with erased clinical symptoms and an abortive course. In such cases, the development of the inflammatory process may stop at the stage of hyperemia, body temperature normalizes within 3-4 days, clinical symptoms subside and the animal recovers.

The diagnosis is based on medical history and characteristic clinical symptoms. X-ray examination reveals extensive, intense foci of shading in the cranial, ventral and caudal areas of the pulmonary field. Sputum microscopy determines the presence of fibrin, leukocytes, erythrocytes, and microbes in the exudate.

Rice. 27. Arc-shaped border of dullness in lobar pneumonia.

Hematologically, neutrophilic leukocytosis with a shift to the left, lymphopenia, and increased ESR are found.

Differential diagnosis. Acute infections are excluded. Lobular pneumonia, unlike lobar pneumonia, occurs with less severe symptoms lung lesions do not have a staged course of the disease and often become chronic.

Acute pneumonia with sweating into the alveoli and bronchioles of rapidly coagulating fibrinous exudate with a high content of red blood cells. The disease is characterized by the cyclical development of the pathological process, the rapid involvement of large areas of the lung (lobar pneumonia). The disease is observed in all animal species, but in its most typical (staged) form it occurs in horses.

Etiology. The causes of lobar pneumonia in horses have not been sufficiently studied. With the same clinical signs, they have two diseases. One of them is highly contagious (contagious equine pleuropneumonia) and is infectious, the other (lobar pneumonia) is not contagious and is considered non-contagious.

Croupous pneumonia as a typical process in the lungs (except for contagious pleuropneumonia) is observed in pasteurellosis, salmonellosis, horse wash, and hemorrhagic disease of horses. It also occurs after overwork, hypothermia, long-term transportation of horses and exposure to other unfavorable factors that reduce the body's resistance.

Clinical signs. The disease suddenly begins with high fever, depression, cough, rapid breathing and difficulty breathing. By auscultation, small and large bubbling wheezes are established (high tide stage); On the second to eighth day, when the exudate released into the lumen of the alveoli coagulates and the flow of air into the alveoli completely stops (hepatization stage), wheezing is no longer audible, but bronchial breathing is detected. Percussion at this stage of pneumonia establishes dullness over a large area of ​​the chest (lobar pneumonia). Its characteristic feature is the curved top (and not horizontal, unlike exudative pleurisy) border. An extensive area of ​​dullness is a very typical sign of lobar pneumonia. But sometimes, when inflammation is localized in the center of the lungs, when the focus is removed from the periphery and for this reason cannot be detected by percussion, extensive dullness is absent.

After 3-4 days from the onset of dullness, moist rales reappear in the lungs, indicating the beginning of the melting of the exudate and its resorption. Percussion at this time establishes the clarification of the percussion sound, i.e. its gradual transition from dull or dull to clear pulmonary (resolution stage). The appearance of wheezing and clearing of the percussion sound indicate the passage of air into the alveoli. Throughout the illness (if no treatment is applied) until the process begins to resolve, the animal maintains a high body temperature (a constant type of fever).

With the beginning of the resorption of the exudate, nasal discharge of a rusty-brown color appears (an admixture of blood breakdown products). Sometimes bleeding is observed at the beginning of the disease. Urine output decreases at the height of the disease, and increases when the resolution stage approaches. Protein, red blood cells, epithelium, and kidneys are often found in the urine, indicating inflammation of these organs.

The activity of the cardiovascular system changes. The pulse quickens. At the beginning of the disease, it is full, strong, the cardiac impulse and the second sound on the pulmonary artery are intensified. With the development of heart failure, edema appears, the filling of peripheral veins increases, the pulse weakens, has a small wave, the first tone is somewhat muffled and stretched out.

Terminology: inflammation of the nasal mucosa is called rhinitis, larynx - laryngitis, trachea - tracheitis, bronchi - bronchitis.

Etiology. There are banal and specific inflammation. The occurrence of banal inflammation of the upper respiratory tract is caused by violations of the technology of keeping and feeding animals. In pigs and cattle, it is associated in most cases with irritation of the mucous membranes when inhaling dusty air and air saturated with ammonia or hot steam. The cause of inflammatory processes is often colds, which reduce the body's resistance to the action of opportunistic microflora, which is always present in the airways. Many infectious and non-infectious diseases are complicated by inflammation of the upper respiratory tract.

Rice. 10. Diphtheritic bovine laryngitis due to necrobacteriosis

Banal inflammation of the upper respiratory tract occurs mainly in the form of serous, serous-mucosal and purulent catarrh. The mucous membrane is swollen, reddened, dotted with hemorrhages, erosions and ulcers. On the surface of the mucous membrane there is serous, serous-mucosal or purulent exudate. Catarrhal inflammation is sometimes accompanied by follicular rhinitis, while the lymphoid follicles are enlarged in size from poppy seeds to peas, as a result of which the nasal mucosa acquires a granular surface. Follicular nodules suppurate, open, and ulcers appear. The chronic course of catarrh ends with the growth of connective tissue. The mucous membrane thickens either diffusely or focally, in the latter case polyps are formed. Less commonly, fibrinous inflammation of the upper respiratory tract develops, which occurs in the form of lobar inflammation and is manifested by the presence of fibrinous-necrotic films; after their separation, ulcers with uneven edges appear. If the outcome is favorable, the ulcers heal. Exudative rhinitis is sometimes complicated by sinusitis and sinusitis, i.e. inflammation of the paranasal cavities. They occur mainly chronically and are manifested by nasal mucopurulent discharge, changes in the configuration of bones in the area of ​​the accessory cavities. Along with banal inflammation, there are rhinitis, laryngitis, bronchitis and tracheitis, which are the main symptom of infectious diseases. This group of diseases includes infectious rhinotracheitis, plague, catarrhal fever of cattle, smallpox, tuberculosis, glanders, and blastomycosis. In these infectious diseases, the mucous membrane of the upper respiratory tract, especially the nasal cavity, is diffusely or focally hyperemic or dotted with nodules, ulcers and fibrinous-necrotic films.

Rice. 11. Bronchitis with nodose peribronchitis of cattle. The lumen of both bronchi is filled with cellular masses. The peribronchial tissue is heavily infiltrated with polymorphonuclear leukocytes and thickened. The alveoli are sharply expanded.

Pneumonia. Inflammation of the lungs is commonly called pneumonia. Pneumonia often affects animals, especially pigs and sheep. Pneumonia often occurs with fatal. According to the localization of foci of inflammation, pneumonia can be lobularia, lobar and acinar. In lobar pneumonia, entire lobes are affected, lobular pneumonia - lobules, acinar pneumonia - acini (the structural unit of the lungs is a bronchiole with a group of adjacent alveoli). Based on their origin, there are banal (simple) pneumonias caused by opportunistic microorganisms present in the airways when the body’s resistance is weakened (colds, overheating, as well as many non-infectious and infectious diseases). There are pneumonias, which are the main symptom of the manifestation of general infectious diseases.

Banal pneumonia occurs predominantly by the exudative type of inflammation. There are two main forms of pneumonia: lobar pneumonia and catarrhal bronchopneumonia.

Lobar pneumonia is a fibrinous inflammation of the lungs, characterized by effusion from the vessels of fibrinogen, which in the lumen of the alveoli is converted into fibrin. The inflammatory process often involves entire lobes of the lung, or at first the pneumonia is lobular and then lobar in nature. Lobar pneumonia occurs in stages: the stage of hyperemia, red hepatization, gray hepatization and outcome (resolution). The hyperemia stage is characterized by redness of the affected lobules or lobes. Under a microscope, dilated and blood-filled interalveolar capillaries are revealed. The lumen of the alveoli contains serous exudate with an admixture of rejected epithelium, a small amount of erythrocytes and leukocytes. Sometimes red blood cells are detected in significant quantities, which corresponds to hemorrhagic exudate. The hyperemia stage is followed by the development of the red hepatization stage. The affected areas of the lung become red in color and resemble the liver in density. Under the microscope, along with hyperemia of blood vessels and interalveolar capillaries filled with serous or serous-hemorrhagic exudate, the admixture of fibrinous exudate is noted. Subsequently, the stage of gray hepatization develops, characterized by the fact that a large number of leukocytes are mixed with the fibrinous exudate. The resulting exudate compresses the capillaries, resulting in ischemia. Externally, the affected area of ​​the lung turns from red to gray, and in density it even more closely resembles the liver. With a favorable course of the disease, the outcome (resolution) stage develops. Leukocytes are dissolved by their enzymes

Rice. 12. Acute lobar pneumonia. G-E.

Rice. 13. Acute lobar pneumonia. Stage of red hepatization. 1- delicate fibrin threads with a small number of leukocytes in the lumen of the alveoli; 2 – area of ​​necrosis of the alveolar wall; 3- sharply injected perialveolar capillaries.

Rice. 14. Lobar pneumonia. Stage of gray hepatization. In the lumen of the alveoli, extensive masses of fibrin are visible, stained pink with eosin. These masses contain a small number of leukocytes and desquamated alveolar epithelium. Empty vessels. Staining G-E.

fibrin, liquefied exudate is absorbed and removed with sputum when coughing, and is partially resorbed by macrophages. The alveoli are gradually freed from exudate, the alveolar epithelium is restored. However, the alveolar septa and stroma layers thicken due to newly formed connective tissue. Thus, even with a favorable outcome of the disease, the lungs lose their elasticity and become denser than normal. A less favorable outcome is that due to thrombosis of blood and lymphatic vessels, necrotic foci are formed in the affected parts of the lung, which undergo organization and carnification, encapsulation or sequestration, or purulent softening. In unfavorable cases, it is complicated by ichorous inflammation. Due to the fact that in some infectious diseases, individual lobules of the lung are not simultaneously involved in the inflammatory process, the surface of the pneumonic area has a variegated color (red, gray-red, gray-white, gray-yellow), reminiscent of a marble pattern - a marbled lung.

Rice. 15. Acute lobar pneumonia with interstitial edema in a cow (marmorated lung). The figure clearly shows areas of the lung in different stages of lobar inflammation. The interstitial tissue is swollen and stands out sharply in the form of thick, swollen cords.

Catarrhal bronchopneumonia characterized by involvement of the bronchi and respiratory tract in the inflammatory process lung tissue. According to localization, lesions can be lobular or lobar. In the acute course of catarrhal bronchopneumonia, the affected area is slightly red in color, slightly swollen above the surface of the organ, and has a consistency similar to the density of the spleen. A cloudy liquid is squeezed out from the surface of the cut, and viscous, grayish-white mucus is squeezed out of the bronchi, stretching into threads. Under a microscope, vascular hyperemia is detected in the affected area of ​​the lung, the alveoli are filled with serous exudate mixed with leukocytes, rejected respiratory epithelium and histiocytes. The lumen of the bronchi is filled with serous cell exudate. The walls of the bronchi are thickened due to cellular infiltration. Bronchial epithelium in a state of mucous degeneration.

The outcome can be favorable, often the exudate resolves, but most of it is removed with sputum when coughing. The lung is restored, however, due to the proliferation of connective tissue, some thickening of the interalveolar and interlobular septa remains. If the course is unfavorable, acute catarrhal bronchopneumonia becomes chronic or becomes complicated purulent inflammation. In chronic catarrhal bronchopneumonia, the affected part of the lung is fleshy, resembles the pancreas in density, and the surface is slightly lumpy. On the red background of the cut surface, gray foci and veins of various shapes are visible, in the center of which the lumen of the bronchi is noticeable. In pigs, the affected lung is white, dense, similar to lard (sebaceous pneumonia). A thick, pus-like mucous mass is squeezed out from the cut surface of the bronchi.

Rice. 16. Acute bronchopneumonia in a calf

Rice. 17. Micropicture of the lung in acute catarrhal bronchopneumonia in a calf. Staining G-E.

Under a microscope, the alveoli are filled with respiratory epithelium, histiocytes, and lymphocytes. In some places, nested accumulations of leukocytes are observed. There is relatively little liquid exudate. The lumen of the bronchi is filled with leukocytes, rejected epithelium and mucus, and bronchiectasis is observed. Granulation tissue with a large number of lymphoid cells and fibroblasts is detected around the bronchi. The layers of interlobular connective tissue and alveolar septa are thickened due to newly formed connective tissue. Necrotic foci without encapsulation and with encapsulation are often found. With a favorable outcome of the disease, complete recovery of the affected part of the lung does not occur; significant growths of connective tissue remain. Catarrhal bronchopneumonia can be complicated by gangrenous inflammation.

Purulent pneumonia develops against the background of catarrhal bronchopneumonia or when pyogenic microbes enter the lungs from purulent foci of other organs (metastatic purulent infection). Therefore, purulent pneumonia occurs either diffusely, in the form of catarrhal-purulent, or in an abscessed form. With purulent-catarrhal bronchopneumonia, the affected part of the lung is compacted, red, and lumpy. The cut surface is red, with a large number of grayish-white lesions with purulent softening in the center. A creamy, thick, viscous mass of exudate is squeezed out of the bronchi.

Rice. 18. Purulent pneumonia. Micro picture. In the lumen of the alveoli and bronchi, a large number of leukocytes and desquamated alveolar epithelium are observed. Purulent exudate fills the lumen of the alveoli and bronchi almost completely.

Lung diseases in animals are divided depending on the nature of the disease into non-inflammatory and inflammatory. Non-inflammatory include hyperemia and pulmonary edema, pulmonary emphysema, and inflammatory ones - pneumonia and gangrene of the lungs.
Emphysema can be alveolar and interstitial, and pneumonia, according to Domrachev’s classification, is divided into lobar (lobar) and lobular (bronchopneumonia, atelectatic, hypostatic, metastatic).

Hyperemia and pulmonary edema - a disease characterized by overflow of blood vessels and leakage of blood plasma into the alveoli and interalveolar tissue.
The causes of active hyperemia and pulmonary edema are sunstroke and heatstroke, hard work in the hot season, inhalation of irritating gases, and passive causes are heart failure, chronic intoxication due to lung diseases and other diseases.

Bronchopneumonia - an animal disease characterized by the development of an inflammatory process in the bronchi and alveoli and the sweating of catarrhal or catarrhal-purulent exudate into the latter. The disease is seasonal, occurring mainly in the late autumn and early spring months. The occurrence of the disease is due to a number of factors. Most often it occurs due to an unfavorable microclimate: high concentrations of ammonia and hydrogen sulfide in the indoor air, severe microbial or dust pollution, the presence of drafts, high humidity, etc. Conditional conditions play a major role in the occurrence of the disease. pathogenic microflora respiratory tract, which, with a decrease in the natural resistance of the body, can be the main etiological factor. Vascular disorders in the lungs play a significant role in the development of the disease, allergic factors, suppression of the protective mechanisms of the respiratory system.

Croupous pneumonia (Pneumonia cruposa) - acute fibrinous inflammation, involving entire lobes of the lung, with pronounced symptoms of allergy and typical changes in the stages of the fibrinous inflammatory process. The disease is diagnosed mainly in horses, less often in other animal species. Recently, most researchers consider lobar pneumonia as a disease of allergic origin, namely as hyperergic inflammation in a previously sensitized organism or sensitized lung tissue. Allergens in this case are microorganisms of the respiratory tract, and irritating gases, hypothermia, trauma, etc. can act as resolving factors. In this case, pneumonia in a sensitized animal develops as a result of exposure to factors of non-antigenic origin (heteroallergy). In addition, microorganisms, both those that participated in sensitization and those that did not participate in it (paraallergy), can be resolving factors. The development of lobar pneumonia occurs in four stages.

First stage - active hyperemia or hot flash - characterized by damming of the pulmonary capillaries with blood; the epithelium covering the alveoli swells and exfoliates, liquid exudate with an admixture of leukocytes and a large number of red blood cells accumulates in the alveoli. There is significantly less air in the affected area than in a healthy one, and by the end of the stage it is completely forced out of the alveoli. The high tide stage lasts from several hours to a day.
Second stage - red hepatization - lasts 2-3 days. At this stage, the alveoli continue to fill with exudate containing red blood cells and fibrinogen. Then the exudate coagulates, as a result of which the alveoli and bronchioles of the affected area are filled with coagulated fibrin with an abundant admixture of red blood cells, deflated epithelium and a small amount of leukocytes.
At the third stage - stage of gray hepatization - migration of leukocytes begins. The number of red blood cells gradually decreases, and the number of white blood cells increases. Under the influence of leukocyte enzymes, fibrin and other components of the exudate are destroyed and take on a gray color. The duration of this stage is 2-3 days.
Fourth stage - resolution stage - characterized by the fact that with an increase in the number of leukocytes, the exudate is broken down and liquefied and thus acquires the ability to be absorbed. The liquefaction of exudate is based on processes occurring under the influence of lipolytic and proteolytic enzymes of leukocytes. Under their influence, fibrin is converted into soluble albumose and amino acids (leucine, tyrosine, etc.). The liquefied exudate is partially absorbed and partially removed with sputum when coughing. Most of the absorbed exudate is excreted in the urine. Air gradually enters the alveoli that are freed from exudate, and at the same time regeneration of the alveolar epithelium occurs. The duration of the stage is from 2 to 5 days.
When opening animals that died from bronchopneumonia, inflammatory foci of various sizes are found in the lungs, colored red-brown, gray-red or gray-white, rising above the surface of the lung. The bronchi contain mucous or mucopurulent exudate. In the chronic course, fibrous fusion of the pulmonary pleura with the costal pleura, and often with the pericardium, is found;
Pathological changes for lobar pneumonia depend on the stage of development of the disease. At the stage of tide, the lung is full of blood and increased in size. The cut surface is smooth and shiny. At the stage of red hepatization, the affected part of the lung is without air, enlarged, resembles a liver in section, and sinks in water. The cut surface is red, granular, due to the fact that the alveoli are filled with coagulated fibrinous exudate and protrude above the cut surface. At the stage of gray hepatization, the lung initially has a gray tint, and at the resolution stage it becomes yellowish. Along with the above-described stage changes, one can detect an increase in bronchial lymph nodes and degeneration of parenchymal organs. At the resolution stage, the lung resembles the spleen in consistency.
Symptoms in acute alveolar emphysema, they manifest themselves as severe shortness of breath, a horn-shaped dilatation of the nostrils when inhaling and protrusion of the anus when exhaling. During auscultation, weakened vesicular breathing is heard, and if the cause of emphysema is bronchitis, wheezing is detected. The posterior border of the lungs is pushed back 1-2 ribs, the percussion sound is boxy.
In chronic alveolar emphysema, expiratory dyspnea is well expressed, exhalation is biphasic. The chest is barrel-shaped. When exhaling, retraction of the intercostal spaces is noted, and an ignition groove is formed along the costal arch. With auscultation, depending on the origin of emphysema, wheezing or weakening of vesicular breathing is detected, and with percussion, an increase in the boundaries of the lungs and a boxy percussion sound.
Interstitial emphysema is acute and develops quickly. Characterized by rapidly increasing shortness of breath and increased heart rate. On auscultation, weakened vesicular breathing and crepitating rales are heard. When air penetrates under the skin, a crepitation noise is detected.
Hematological examination in horses can reveal an increase in the number of red blood cells and hemoglobin.
The first symptoms of bronchopneumonia are characterized by depression of the animal, general weakness, body temperature usually rises by 1-2 °C, and scant serous-mucosal or mucopurulent discharge is observed from the nasal cavities. Shortness of breath is usually mixed type. The mucous membranes are cyanotic. Breathing is shallow, rapid, tachycardia. When auscultating the chest, hard vesicular breathing, fine rales are heard, and sometimes bronchial breathing can be heard. On percussion there are areas of dullness. The cough is initially dry and painful, but later becomes moist and less painful.
Hematological examination in patients with bronchopneumonia reveals neutrophilic leukocytosis with a shift of the nucleus to the left to myelocytes, lympho- and eosinophilia, monocytosis, decreased acid capacity, blood serum, accelerated ESR, decreased hemoglobin content.
Lobar pneumonia begins suddenly. The onset of the disease is characterized by quickly appearing depression of the animal, refusal of food, and increased thirst. At slight movement shortness of breath and painful cough appear. The temperature rises to 41-42 °C and remains at this height for 6-8 days with minor daily fluctuations, i.e. the type of fever is constant. In its clinical manifestation, three stages are distinguished: hyperemia, hepatization and resolution. Typical symptom Lobar pneumonia at the onset of the disease is a discrepancy between the increase in body temperature and the increase in heart rate. If the temperature rises by several degrees, then the pulse during this period increases by 10-15 beats. The high temperature usually lasts until the end of the hepatization stage (6-8 days), and then either drops to normal within 12-36 hours (crisis), or reaches normal gradually over 3-6 days (lysis). Visible mucous membranes are icteric, sometimes lemon-yellow. These phenomena are soon joined by symptoms specific to lobar pneumonia, which vary depending on the stage of the disease.
During percussion at the first stage, a tympanic sound is established in the affected lobe, which during the period of hepatization becomes dull and dull. Dullness can be of different sizes, its boundaries have different shape, however, the upper border is always arched upward. At the resolution stage, the percussion sound acquires a tympanic hue, and as the normal state of the lung tissue is restored, it becomes clear, atympanic.
During auscultation at the stage of hyperemia, increased vesicular breathing is initially detected, and by the end of the stage, crepitating fine bubbling rales are heard during the inhalation phase. With the development of the hepatization stage, wheezing disappears, a gradual disappearance of vesicular breathing and the appearance of bronchial breathing are established, sometimes respiratory sounds in the lesion are not audible at all. At the resolution stage, rough, moist rales are heard, which become more and more numerous and drown out bronchial breathing. Then the sonority of wheezing gradually decreases, bronchial breathing weakens and turns into normal vesicular noise.
A characteristic symptom of lobar pneumonia is the appearance of saffron-yellow or rusty-brown nasal discharge at the stage of hepatization. It is observed before the resolution stage begins.
Certain changes in lobar pneumonia are observed in the activity of the cardiovascular system. From the very beginning of the disease, the pulse is increased, but this increase is not proportional to the increase in body temperature (the temperature rises by 3-4 ° C, and the pulse increases by 10-15 beats). This discrepancy is typical for initial stage diseases. Heart sounds are usually loud, clear, the 2nd tone is often accentuated. A significant increase in heart rate, weakness and arrhythmia with a sharp drop in blood pressure indicate developing cardiovascular failure. It should be noted that the degree of cardiac dysfunction is usually directly proportional to the degree of damage to the lung tissue.
Croupous pneumonia is accompanied by functional disorders in the activity of the urinary and digestive systems. Neutrophilic leukocytosis, lymphopenia, eosinopenia, and increased ESR are detected in the blood.
Diagnostics diseases of animals with hyperemia and pulmonary edema are carried out on the basis of anamnesis and clinical manifestation. In differential terms, one should keep in mind heat stroke, poisoning and intoxication.
Diagnosis of emphysema diagnosed on the basis of anamnesis and characteristic clinical symptoms (progressive shortness of breath, cyanosis of the mucous membranes, biphasic inhalation, horn-shaped dilatation of the nostrils, the presence of an ignition groove, box percussion sound), and in the case of interstitial - very rapid development of the disease, crepitating rales, the presence of subcutaneous emphysema in the neck , chest, back. Emphysema should be differentiated from pneumonia and pleural diseases (pleurisy, hydrothorax and pneumothorax).
When diagnosing bronchopneumonia take into account data from anamnesis, clinical manifestations, and laboratory tests. Infectious and invasive diseases occurring with respiratory syndrome, as well as lobar pneumonia and other lobular pneumonia.
Animal disease with lobar pneumonia is diagnosed taking into account the analysis of anamnestic data (suddenness of the disease), characteristic clinical signs (persistent fever, saffron yellow fibrinous discharge from the nasal cavities, stages of disease development, damage to the entire lobe of the lung with the superior arcuate line), and laboratory blood tests. At differential diagnosis such infectious diseases, such as contagious pleuropneumonia of horses, peripneumonia of cattle, swine influenza, etc.
Treatment animals suffering from pulmonary congestion should be treated urgently. To prevent the development of pulmonary edema, bloodletting is done (0.5-1% of body weight). Shown intravenous administration 10% solution of calcium chloride 100-150 ml or intramuscular - calcium gluconate 40-50 ml in a 10% solution, hypertonic solutions of glucose and sodium chloride can be administered intravenously. At the same time, the animal is given heart medications and the chest is rubbed. Good results obtained from novocaine blockade of the stellate or lower cervical sympathetic nodes.
When treating sick animals alveolar emphysema lungs, to reduce shortness of breath, it is also recommended to use sedatives such as chloral hydrate (30.0-40.0 g) with a mucous decoction in the form of small enemas, bromide preparations orally (10.0-30.0 g 3-4 times a day) or intravenously 10% solution, in a dose of 100-150 ml for a week in horses. For the same purpose, a 0.1% solution of atropine or a 5% solution of ephedrine is injected subcutaneously daily for 5-7 days (horses, 10-15 ml per injection), euphilin 0.1-0.2 g is used orally appointment. Treatment of patients with interstitial emphysema involves giving them rest, using cardiac medications, antitussives, and solutions of atropine or ephedrine.
The highest effectiveness in the treatment of animals with bronchopneumonia is obtained with timely initiation of complex therapy for patients with acute course diseases. First of all, optimal feeding and housing conditions should be created for the animals. Among the means of etiotropic therapy, antibiotics are prescribed taking into account the sensitivity of the respiratory tract microflora to them. It is advisable to use antibiotics in combination with sulfonamides. The latter are prescribed orally, and soluble sulfonamide salts can also be used intravenously. Antibacterial drugs can also be administered in the form of aerosols. For this purpose, antibiotics are used, which are administered on average at 400,000-500,000 units/m3, iodinol - 2 ml/m3, camphor serum according to Kadykov - 15 mg/m1, etc. Among the means of pathogenetic therapy, nonspecific stimulating drugs (gamma- globulins, nonspecific polyglobulins, hydrolysin, hemotherapy), regulating neurotrophic functions (novocaine blockade of the stellate ganglion or splanchnic nerves and sympathetic trunks according to Shakurov), antiallergic and symptomatic agents.
Treatment of animals with lobar pneumonia begins with their isolation. At the first stage of the disease, in order to reduce hyperemia of the lungs, it is recommended to carry out bloodletting (in horses 2-3 l), from antibacterial agents antibiotics and sulfonamides are used. Before use, determine the most active drug according to the sensitivity of the respiratory tract microflora to it. The most commonly used antibiotics are penicillin, streptomycin, tetracycline, oxytetracycline, and new ones are cephalosporins, aminoglycosins, and hipols. Antibiotics are used 3-4 times a day for 8-10 days, in doses depending on the type of animal and its weight. Among the means of pathogenetic therapy, antiallergic drugs (diphenhydramine, sodium thiosulfate, sodium chloride, suprastin, pipolfen, etc.), novocaine blockade of the stellate or lower cervical sympathetic ganglion, rubbing the chest with irritating ointments, cupping, etc. are used. symptomatic therapy use cardiac, expectorant, diuretics.
Warning animal diseases with hyperemia and pulmonary edema is to organize correct mode operation, protection from overheating, inhalation of irritating and toxic gases. Preventive measures for the occurrence of pulmonary emphysema are also nonspecific and are aimed at proper operation and especially timely and full treatment bronchitis.
Prevention animal diseases of bronchopneumonia should include a complex of economic, zootechnical and veterinary measures. Constant monitoring of the microclimate of animal premises is necessary, balanced diet for all major nutrients and vitamins, especially in relation to vitamin A. In the conditions of industrial complexes, one should strictly adhere to the rules for their acquisition (the smallest number of supplying farms, anti-stress treatments, rational formation of groups, adherence to the principle “everything is empty - everything is occupied”, etc.). Pharmacotherapy includes drugs that increase the body’s natural resistance, including physiotherapy (aeroionization, ultraviolet irradiation).