home Endocrinology Lobar pneumonia in horses. Analysis of literature data. Pneumonia in a dog is accompanied by

Lobar pneumonia in horses. Analysis of literature data. Pneumonia in a dog is accompanied by

Lobar pneumonia (Pneumonia crouposa) is an acute febrile disease characterized by acute lobar (fibrinous) inflammation, involving entire lobes of the lung, with pronounced allergy symptoms and typical changes in the stages of the fibrinous process.

Lobar pneumonia affects mainly horses, less often sheep and young cattle. Among animals of other species, lobar pneumonia is rarely recorded. In emaciated and weakened animals, lobar pneumonia occurs in an atypical form and is more similar to catarrhal bronchopneumonia. IN last years in specialized farms for raising heifers and fattening calves, a significant increase in the incidence of disease in calves is recorded 1-3 one month old serous-fibrinous and fibrinous-purulent pneumonia.

Etiology. In the occurrence of lobar pneumonia in animals, the main role belongs to two factors: the allergic state of the body and pathogenic microflora. Lobar pneumonia in animals can be caused by various gram-positive, gram-negative microorganisms, virulent strains of pneumococci, diplococci, mycoplasma, chlamydia, pasteurella, fungi, and viruses. Pneumonia in animals can be caused by microbial association. When conducting a study of nasal discharge, tracheal contents and material from pneumonic areas of the lungs in a veterinary laboratory, staphylococci, streptococci, pasteurella, chlamydia and other microbes are isolated. At the same time, the listed microorganisms can sometimes be isolated from healthy animals.

Many researchers associate the occurrence of lobar pneumonia with increased allergic reaction body caused by a strong irritant - stress. This condition in animals can develop after sudden hypothermia of a horse that is hot after a competition, driving sheep in hot weather through cold mountain rivers, or quickly transferring cattle from a warm, stuffy room to a damp and cold one.

Pathogenesis. As a result of the influence of factors unfavorable for the animal on the receptor apparatus of the respiratory organs, a number of deviations occur in the animal’s body. In the body of a sick animal, a disturbance in the neurovascular reaction occurs, phagocytic protective forces and immunobiological processes decrease, as a result of which more favorable conditions for the development of pathogenic and conditionally pathogenic microflora. The main route of infection of the respiratory tract is aspiration of nasopharyngeal secretions, the aerogenic route, or hematogenous and lymphogenous transfer of microorganisms from extrapulmonary foci to the lower respiratory tract. In this case, inflammation develops, which usually begins in the depths of the lobe; inflammation, mainly through the lymphatic tract, quickly spreads to the periphery of the lung, capturing large areas of the lung. In animals, lobar inflammation most often develops in the cranial or ventral parts of the lungs, less often in the caudal lobe and even less often in the dorsal parts of the lung.

In the development of pneumonia, disturbances in the local lung defense system, incl. decrease in mucopillar clearance, activity of alveolar macrophages and neutrophils, secretory immunoglobulins.

Damage to local defense mechanisms against the background of a decrease in the resistance of the animal’s body creates favorable conditions for the activation of the microbial flora and the occurrence of pneumonia.

Croupous pneumonia is characterized by pronounced stages (first, hyperemia occurs in the lungs, then the stage of red and gray hepatization and ends with the stage of resolution).

The first stage (stage of inflammatory hyperemia, hot flash). At this stage there is a strong expansion blood vessels and their overflow with blood, desquamation of the alveolar epithelium. This stage in an animal it lasts from several hours to a day. They are secreted into the lumen of the alveoli viscous exudate, leukocytes and erythrocytes, the animal’s oxygen exchange becomes difficult, urination and heat regulation are disrupted.

In the second stage (red hepatization stage), the exudate in the alveoli, infundibulae and bronchioles coagulates, the lung tissue thickens and takes on the appearance of a liver. Through the affected area of the lung, the flow of oxygen into the blood and the release of carbon dioxide from the blood stops.

In the second stage, the use of oxygen by tissues, the oxidation of carbons, and the flow of glucose into the brain decreases. As a result of all this, oxygen deficiency sharply manifests itself in the animal’s body, intoxication increases, despite significant heat transfer, and a further increase in body temperature occurs. In the blood of a sick animal, the amount of intermediate breakdown products, unconverted bilirubin and leukocytes increases. Part of the uncoagulated exudate and lysis products ends up in Airways healthy areas of the lung, causing their irritation, and is released from the nose in the form of a saffron-yellow discharge.

Third stage (gray hepatization stage). The coagulated exudate, under the influence of leukocytes and other factors, undergoes fatty degeneration, intoxication increases, the formation of unresolved bilirubin and the penetration of the latter into tissues, and the secretion of saffron-yellow discharge from the nose increases. When fatty degeneration reaches a high degree, the lung tissue itself acquires a yellow color. Because of this, some scientists sometimes call this stage the yellow hepatization stage. At this stage, the increase in body temperature and intoxication of the body reach the maximum degree in the sick animal. The second and third stages in sick animals last 2 days.

During the development of lobar pneumonia in a sick animal, pulmonary respiration, the amount of oxygen in the blood of a sick animal decreases by 30-50%. At the same time, the absorption of oxygen from the blood by tissues in the body decreases, which leads to worsening hypoxia, disruption of redox processes in tissues and organs, and the amount of intermediate decay products in the body increases. In the blood, the amount of albumin, beta and gamma globulins, tryptophan, and eosinophils decreases, reserve alkalinity and blood pH decrease, and the number of red blood cells, sugar, and carbon dioxide increases.

Fourth stage (resolution stage). At this stage, under the influence of lipolytic enzymes secreted by leukocytes, the exudate liquefies. A large number of lysis products are absorbed into the blood and released through the respiratory tract, the flow of air into the alveoli is restored, the epithelium is regenerated, the animal’s urination increases, and the number of eosinophils and chlorine in the blood increases. The resolution process in the body of a sick animal lasts up to 7 days.

In some animals with lobar pneumonia, loss of one of the characteristic symptoms. Therefore, six additional atypical forms of the disease are identified: abortive, which occurs in strong animals and occurs within 1-2 days; creeping, when the process spreads in the lungs; recurrent, which develops again in recovered animals; senile; central when inflammatory process localized in the center of the lung; massive, capturing the entire lobe.

Clinical picture. In most animals, lobar pneumonia is acute. The disease in animals begins with severe chills, a rapid rise in body temperature to 41-42°C, sudden depression and weakness, increased breathing and mixed shortness of breath. The animal's productivity drops sharply. On clinical examination, the mucous membranes of a sick animal are hyperemic and icteric. Sick animals cough, starting from the second day of illness and until the 2-3rd day of the resolution stage, a saffron-yellow discharge is released from the nasal openings. The heartbeat is increased, the pulse is accelerated, hard; vascular filling is increased. The ratio between the number of respiratory movements and pulse waves instead of 1:2-3 (in healthy animals) becomes 1:1. During the flushing stage, when auscultating the lungs in the affected areas, we listen to hard vesicular breathing and sounds of crepitus. In the stage of hepatization, there are no respiratory sounds during auscultation; we can detect weak bronchial breathing. At the stage of resolution of the process, when the alveoli are freed from exudate, during auscultation we again listen to the sounds of crepitus, which after 1-2 days are replaced vesicular respiration. When percussing the lungs in the stage of inflammatory hyperemia, we get a loud sound with a tympanic tint; in the stage of hepatization, the sound becomes dull or dull in a large part of the lung (more often than one). A dull sound during percussion in animals is heard by a veterinarian behind the shoulder blades and in a caudal direction from it. In the resolution stage, the tympanic shade of the pulmonary sound appears again.

At the site of the affected lobe, fluoroscopy reveals foci of darkening, and radiography reveals clearing.

At the onset of the disease, there is a slight increase in heart rate that does not correspond to body temperature (with an increase in temperature by 2-3°C, the pulse increases by 10-15 beats). This situation is typical for lobar pneumonia. Subsequently, as pneumonia develops, veterinary specialists note a significant increase in heart rate, arrhythmia and symptoms of myocarditis. In cases of prolonged illness or complications, the pulse quickens, becomes weaker and softer. The veins become more tortuous and filled with blood.

In this case, the degree of cardiac dysfunction usually corresponds to the degree of lung damage. Sometimes, during a period of critical drop in temperature, a sick animal develops vascular insufficiency: it drops sharply muscle tone, peripheral veins become empty, visible mucous membranes become pale, peripheral parts of the body are cold, the pulse becomes thready, heart sounds are weakened, and blood pressure drops. When examining an animal, it disappears conditioned reflexes, reflexes of the cornea and skin decrease.

A sick animal has a decreased appetite, gastrointestinal peristalsis intestinal tract slow, gastritis and coprostasis are recorded. Diuresis in the hepatization stage is reduced, and with the onset of the resolution stage it increases. When examining the blood, we find a sharp neutrophilic leukocytosis with a shift to the left, lymphopenia, anesinophilia and monopenia, a decrease in the number of platelets and red blood cells. With the resolution of lobar pneumonia, the morphological and biochemical composition of the blood is restored.

With an atypical course of the disease, which more often occurs in cattle, sheep, weakened and emaciated animals, the clinical symptoms of lobar pneumonia are very diverse. The duration of lobar pneumonia can vary from several days to several weeks. Fever during illness can become remitting. Animals, after apparent recovery, often experience relapses of the disease.

Flow. The duration of lobar pneumonia depends on feeding conditions, maintenance, body condition, timeliness of treatment started and compliance with the course of treatment.

Timely initiation of treatment for good conditions maintenance and proper feeding can interrupt the inflammatory process in the lungs at the first stage of its development. In practice, most cases of lobar pneumonia last for 14-15 days, and sometimes more. A longer course of the disease occurs with complications of the disease: exudative pleurisy, hepatitis, gangrene of the lungs, degenerative changes in the heart and kidneys, and encephalitis.

The prognosis of the disease depends on the condition of the body, the location of the lesion and the duration of the course. A more favorable prognosis occurs when the disease is complicated by exudative pleurisy, hepatitis, a less favorable prognosis occurs when the upper third of the lung and near the diaphragmatic area are affected.

Pathological changes. Each stage of development of lobar pneumonia is characterized by its own pathological changes.

The first stage is accompanied by hyperemia, blood stasis, slight leakage of fluid into the alveoli and interstitial space of the lung tissue. The affected lobe of the lung is slightly increased in volume, has a dark red color, is rather dense to the touch, in the lumen of the pulmonary alveoli, except serous fluid, does not contain a large number of red blood cells

In the red hepatization stage, the alveoli are completely filled with a coagulated red mass. The affected lobe of the lung is airless and resembles the liver in consistency and color.

In the stage of gray hepatization, fibrinous exudate contains a large number of leukocytes and reflexed alveolar epithelium.

In the stage of yellow hepatization, the lung tissue is dense and has a yellow tint; in the lumen of the bronchi we find a large amount of dense and a small amount of liquid mass of saffron-yellow color.

The resolution stage is characterized by the filling of the alveoli with yellow exudate; in some dead animals we find growth of connective tissue and death of the alveolar tissue.

Diagnosis Lobar pneumonia is diagnosed on the basis, as is customary among doctors, of the “gold standard” - high constant fever, cough, sputum, severe neutrophilic leukocytosis with a shift to the left, leukopenia, accelerated ESR. In the nasal discharge and tracheal mucus, fibrin, leukocytes, erythrocytes, and microbial bodies are found in the exudate. X-rays reveal extensive intense foci of shading in the cranial, ventral and central areas of the pulmonary field. At the same time, the intensity of shading is most pronounced in the stages of red and gray hepatization.

Differential diagnosis. When carrying out differential diagnosis, the veterinarian must first of all exclude acute infectious diseases, occurring with lung damage: contagious pleuropneumonia of horses, infectious pneumonia of sheep and goats, mycoplasmosis and others. For this purpose, it is necessary to carry out an analysis of the epizootic situation and a set of special laboratory diagnostic studies, including isolation from exudate and identification of microbial pathogens.

Lobar pneumonias from lobar pneumonias are excluded by the fact that they occur with less severe symptoms lung lesions, they do not have the staged development of the disease characteristic of lobar pneumonia.

We exclude pleurisy, hydrothorox and pneumothorax by auscultation, percussion and the absence of high body temperature in the sick animal. In doubtful cases, it is necessary to conduct an X-ray examination or make a diagnostic puncture pleural cavity(thoracentesis).

The prognosis for lobar pneumonia is usually cautious, and if there is a delay in providing the animal with qualified veterinary care often unfavorable.

Treatment. Veterinary specialists should consider animals that have symptoms inherent in lobar pneumonia as suspicious for a particular infectious disease. Based on this, such animals must be promptly isolated in a separate room or isolation room, and the room where the animals were must be thoroughly disinfected.

When organizing the treatment of an animal with lobar pneumonia, a veterinary specialist should set himself the following tasks:

- provide the sick animal with an easily digestible, complete diet.

- reduce oxygen deficiency.

— delay the development of pathogenic microflora in the lung tissue.

- create an outflow of blood from the lung tissue affected by inflammation.

- normalize neurotrophic processes in the affected area lung tissue.

- take measures to resolve and remove accumulated exudate.

In summer, in good calm weather, it is better for owners of sick animals to keep them under shady canopies or in the shade of trees. Herbivores are given fresh green grass and vitamin hay in their diet. The water should be at room temperature. The diet of carnivores should consist of strong meat broth and finely chopped pieces of fresh meat.
Treatment of a sick animal begins with active antibacterial therapy; from the first hours of illness, novarsenol, miarsenol, antibiotics or sulfonamide drugs are used.

Novarsenol is administered intravenously to a sick animal in the form of 10% aqueous solution 1 time per day or every other day until complete clinical recovery at a dose of 0.005-0.01 dry substance of the drug per 1 kg of animal body weight. Miarsenol is used intramuscularly in the same doses.

Antibiotics after titration of pulmonary exudate for sensitivity in a veterinary laboratory - penicillin, streptomycin, tetracycline, terramycin, oxytetracycline, neomycin sulfate and others are administered intramuscularly 3-4 times a day for 8-10 days in a row at a dose of 5000-7000 U/kg, Bicillin-3, 5. Recently, they have also been used modern antibiotics cephalosporin series.

Sulfonamide drugs (norsulfazole, sulfadimezin, etazol, sulfadimethatoxin and others) are administered to sick animals with food 3-4 times a day for 7-10 days in a row at a rate of 0.02-0.03 g/kg.

Along with antibacterial drugs, sick animals are treated with pathogenetic therapy: unilateral blockade of the lower - cervical sympathetic nodes (alternately every other day on the right and left sides), rubbing the chest wall with turpentine or 5% mustard alcohol, for calves and small animals, jars are placed on the lateral surfaces of the chest wall. Used daily as antiallergic therapy intravenous injections for 5-6 days in a row, sodium thiosulfite at the rate of 300-400 ml of a 30% aqueous solution per administration to a large animal (cow, horse), 10% calcium chloride solution at 100-150 ml per administration (cow, horse).

To relieve intoxication in a sick animal, a 20-40% solution of glucose with ascorbic acid, a 10% solution of sodium chloride or hexamethylenetetramine in therapeutic doses. At the same time for normalization carbohydrate metabolism and reduce intoxication, insulin is administered simultaneously with the glucose solution.

Support of cardiac activity plays a significant role in the successful treatment of lobar pneumonia; with the development of symptoms of cardiac vascular insufficiency sick animals are given injections of camphor oil, caffeine, camphor-alcohol solutions, strophanthin, cordiamine, and adrenaline are administered intravenously in therapeutic doses. When oxygen deficiency (hypoxia) develops, oxygen therapy is administered.

In the resolution stage, expectorants are used for a sick animal: ammonium chloride 7-15g, sodium bicarbonate -20g 3 times a day, and diuretics - juniper berries - 20-50g, furosemide - 0.4, diacarb -1.5-2, timisol - 5-10, hypothiazide - 0.25 - 0.5, potassium acetate -25-60, bearberry leaves -15 -20, hexamethylenetetramine (urotropine) orally and intravenously 5-10 g 2 times a day for 3-4 days.

When treating sick animals, autohemotherapy, diathermy, ultra-high frequency therapy, and warm wraps are used. chest, heating the chest with incandescent lamps and other means.

At high temperature antifibrin is given inside the body - 15-30g, phenacytin -15-25g, latophenine - 10-15g. A sick animal can be given a short-term cold shower, followed by active rubbing of the body, warm wrapping and keeping the patient in a room with an air temperature of about 20°C.

For large animals (horses), alcohol therapy is used (33% alcohol in a vein up to 200 ml).

After clinical recovery, the animals are kept in a hospital for at least 7-10 days under the constant supervision of a veterinary specialist. During this period, horses are released from work and training.

Prevention. Prevention of lobar pneumonia is based on strengthening the body's resistance, compliance by animal owners with the technology of keeping and proper use of sports and working horses. Owners should not allow animals to become hypothermic, especially after being in warm and stuffy rooms or during transportation. It is forbidden to give water to hot animals cold water and leave in cold wind and draft. Animal owners must comply with the deadlines and rules for mechanical cleaning and disinfection of premises, and promptly sanitize stalls and boxes.

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 abscess...

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PAGE 16

Bronchopneumonia (catarrhal pneumonia) Bronchopneumonia - - - 3
Clinical and anatomical forms of pneumonia - - - - - - - - - - - - - - - - - - - - - -4
Etiology catarrhal bronchopneumonia - - - - - - - - - - - - - - - - - - - - - 9
Pathogenesis of catarrhal bronchopneumonia - - - - - - - - - - - - - - - - - - 10
Symptoms of catarrhal bronchopneumonia - - - - - - - - - - - - - - - - - - -12
Pathomorphological changes in catarrhal bronchopneumonia - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -13
Diagnosis and differential diagnosis of catarrhal bronchopneumonia - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - 15
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 the medical history, etiological factors, clinical picture and results of a 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 in 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 serous exudate (inflammatory edema) begins to leak from the walls of the capillaries into the lumen of the alveoli. 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 often initial process 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. In this case, the lung tissue turns dark red or gray, becomes dense in consistency, and the pieces sink in 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 increases from severe swelling 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, 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. When opened, the sequester can be completely removed and it can be distinguished anatomical structures lung 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 of 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 leukocytes that accumulate over time undergo degenerative changes and turn into purulent bodies. Exudate rich in protein and cellular elements accumulates in the alveoli.

Hemorrhagic pneumoniacharacterized by the predominance of a large number of red blood cells in the exudate. It is observed in a number of infectious diseases (anthrax, swine fever), which occur with a violation of the integrity of the walls of blood vessels and the 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. 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 a secondary disease that accompanies other diseases. It has a polyetiological basis and arises as a result of the complex effect on the body of various types of unfavorable factors, in particular, the weakening of the immune status of animals as a result of stress, hypothermia, overheating, inhalation of polluted air, inadequate feeding, etc. The disease usually accompanies canine distemper, hemorrhagic septicemia 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, constantly present in the respiratory tract or viral and bacterial infection, 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 causes may also be the entry of foreign particles and feed into the alveoli, often leading to the development of a special catarrhal inflammation of the 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.

In a 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 erythropoiesis. 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 dyspnea, 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 of the 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

When opening the 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, as well as enlarged bronchial lymph nodes, are often detected. From nonspecific changesin the chronic form of the disease, exhaustion, dystrophy of the myocardium, liver, kidneys, and muscle atrophy occur.

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 given clinical symptoms, taking into account the anamnesis, etiological factors and relevant special research methods, 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 mass diagnosis of bronchopneumonia in calves, sheep, pigs in general and especially in large livestock farms R. G. Mustakimov proposed a fluorographic method.

In particularly 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 the differential diagnostic relation, one should exclude bronchitis, other pneumonia, especially lobar, as well as infectious and invasive diseases accompanied by damage to the 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.

Croupous 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 of agriculture. 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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Lung diseases in animals are divided depending on the nature of the disease into non-inflammatory and inflammatory. Non-inflammatory ones include hyperemia and edema of the lungs, emphysema, and inflammatory ones include 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, hydrogen sulfide in the indoor air, severe microbial or dust pollution, the presence of drafts, high humidity, etc. A major role in the occurrence of the disease is played by conditionally pathogenic microflora of the respiratory tract, which, when the natural resistance of the body decreases, may 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 mucous purulent 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 of a 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. With slight movement, shortness of breath and a 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 upper limit always arched upward. At the stage of resolution, the percussion sound acquires a tympanic connotation, and as it recovers normal condition In the lung tissue it becomes clear and 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 the initial stage of the disease. 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.
Lobar 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 Animal diseases with hyperemia and pulmonary edema are carried out on the basis of anamnesis and clinical manifestations. 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 the history, clinical manifestations, laboratory research. Infectious and invasive diseases occurring with respiratory syndrome, as well as lobar pneumonia and other lobular pneumonia should be excluded.
Animal disease with lobar pneumonia is diagnosed taking into account the analysis of anamnestic data (suddenness of the disease), characteristic clinical signs(permanent 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), laboratory blood tests. At differential diagnosis Infectious diseases such as contagious equine pleuropneumonia, bovine peripneumonia, swine influenza, etc. should be excluded.
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). Intravenous administration of a 10% solution of calcium chloride 100-150 ml or intramuscular administration of calcium gluconate 40-50 ml in a 10% solution is indicated; 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 are obtained from novocaine blockade of the stellate or lower cervical sympathetic nodes.
When treating animals with alveolar pulmonary emphysema, 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, orally bromide preparations (10.0-30.0 g 3-4 times a day) or intravenously 10% solution, at 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.
Most high efficiency in the treatment of animals with bronchopneumonia, obtained when promptly started complex therapy 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, the most active drug is determined by 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 the correct operating mode, protect against overheating, and inhalation of irritating and poisonous 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. It is necessary to constantly monitor the microclimate of the premises for animals, a balanced diet of all essential nutrients and vitamins, especially vitamin A. In 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, compliance with the principle “everything is empty - everything is occupied”, etc.). Pharmacotherapy includes drugs that increase the body’s natural resistance, including physiotherapy (aeroionization, ultraviolet irradiation).

Lobar pneumonia(Pneumonia crouposa)

Lobar pneumonia- acute, cyclical developing inflammation lungs, covering an entire lobe or a significant part of it, in which fibrinous exudate, leukocytes and erythrocytes sweat into the lumen of the alveoli and bronchi, a high fever of a constant type is expressed, and a saffron-yellow discharge is released from the nasal openings. It can be sporadic and massive, primary, secondary and symptomatic.

Etiology. Massive lobar pneumonia manifests itself as one of the main symptoms of peripneumonia and gbmosepticemia.
Sporadic lobar inflammation of the Lungs often occurs with hypothermia, overwork, the presence of a “critical” amount of saprophytic microflora in the respiratory tract, allergies, overirritation of the central nervous system, damage to nerve nodes, severe irritation of N. phrenicus, N. ischiadicus, disruption of the integrity of the trunks of the Sympathetic and parasympathetic nervous system , metabolic disorders (more often with diabetes).

Pathogenesis. When extra- and interoreceptors are exposed to unfavorable factors, a number of deviations occur. The neurovascular reaction is disrupted, phagocytic-protective forces and immunobiological processes are reduced, thereby creating more favorable conditions for pathogenic and conditionally pathogenic microflora. Microflora aerogenously or hematogenously and lymphogenously penetrates into the lower parts of the respiratory tract, contributes to the development of inflammation, which usually begins in the depths of the lobe, then quickly spreads mainly through the lymphatic ducts to the periphery and covers large areas of the lung. The pathological process develops more often in the cranial or ventral parts of the lungs, less often in the caudal lobe and even less often in the dorsal parts of the lung. The development of inflammation is characterized by stages, that is, hyperemia occurs first, then the stage of red and gray hepatization and ends with the stage of resolution.
In the stage of hyperemia, a strong dilation of blood vessels and their overflow with blood occurs, sloughing of the alveolar epithelium. Viscous exudate, leukocytes and erythrocytes are released into the lumen of the alveoli, oxygen exchange becomes difficult, urination and heat regulation are disrupted. Leukocytosis appears, eosinophils disappear. This stage lasts from several hours to a day. In the second stage - red hepatization - the exudate coagulates, the lung tissue thickens and takes on the appearance of a liver. Through the affected area, the flow of oxygen into the blood and the release of carbon dioxide from the blood stop.
In addition, the use of oxygen by tissues, the oxidation of carbons, and their entry into the brain are reduced. As a result of the current conditions, oxygen deficiency sharply manifests itself, intoxication increases, and body temperature rises to an even greater extent, despite significant heat transfer. In the blood, the amount of intermediate breakdown products, unconducted bilirubin and leukocytes increases. Part of the uncoagulated exudate and lysis products enters the respiratory tract of healthy areas of the lung, irritates them and is released in the form of a saffron-yellow discharge.
In the stage of gray hepatization, the coagulated exudate under the influence of leukocytes and other factors undergoes fatty degeneration, intoxication, the formation of unconducted bilirubin and the penetration of the latter into tissues increase, and the discharge of saffron-yellow discharge from the nose increases. When fatty degeneration reaches a high degree, the lung tissue becomes yellow in color. Some authors call this stage the stage of yellow hepatization. In the stage of yellow hepatization, intoxication and fever reach their maximum degree (critical condition). The second and third stages last for 2 days.
In patients during the development of lobar pneumonia, pulmonary respiration is impaired, which leads to a decrease in the amount of oxygen in the blood by 30-50%. At the same time, the absorption of oxygen by tissues decreases, which leads to worsening hypoxia, disruption of redox processes in organs and tissues, and an increase in intermediate decomposition products. In the blood, the amount of albumin, beta and gamma globulins, tryptophan, eosinophils decreases, reserve alkalinity and pH decrease, the number of red blood cells, sugar, and carbon dioxide increases. In the resolution stage, increased liquefaction of the exudate occurs under the influence of lipolytic enzymes secreted by leukocytes; a large number of lysis products are absorbed into the blood and released through the respiratory tract, the flow of air into the alveoli is restored, the epithelium is regenerated, urination increases, the number of eosinophils and chlorine in the blood increases and the content of other substances is normalized. The permitting process lasts up to 7 days.
Sometimes with lobar pneumonia one of the characteristic symptoms disappears. Therefore, six atypical forms of the disease are distinguished: abortive, which occurs in strong animals and lasts 1-2 days; creeping, when the process spreads in the lungs; recurrent, which develops again in recovered animals; senile; central, when the process is localized in the center of the lung; massive, capturing the entire lobe.
Symptoms The disease begins with a rapid rise in body temperature to 41-42 °C, depression of the general condition, and a sharp drop in productivity. Patients cough. A saffron-yellow discharge is released from the nasal openings, starting from the second day of illness until the 2-3rd day of the resolution stage. There is a significant increase in cardiac impulse and increased heart rate. The ratio between the number of respiratory movements and pulse waves instead of 1: 2-3 (in healthy animals) is 1: 1.
When auscultating the chest in the stage of congestion, crepitus and hard vesicular breathing are heard in the affected areas, mainly in the lower third, less often in the middle third of the chest. In the stage of hepatization, there are no respiratory sounds, and weak bronchial breathing appears. At the stage of resolution of the process, when the alveoli are freed from exudate, crepitation noises reappear, followed after 1-2 days by vesicular breathing. The percussion sound changes in accordance with the stages of the inflammatory process: in the stage of influx - tympanic, in the stage of hepatization - dull or dull, in the stage of resolution - tympanic.
With fluoroscopy, foci of darkening are found at the site of the affected lobe, and with radiography, clearing is found. Changes from the side of cardio-vascular system occur from the first days of illness. An increase in body temperature by 1 °C is accompanied by an increase in heart rate by 10-20 waves per minute. The pulse becomes full, at this time the heartbeat also increases. Heart sounds are clear, but amplified, especially the second one on the pulmonary artery. In cases of prolonged illness or complications, the pulse quickens, becomes weaker and softer. The veins become more tortuous and filled with blood, the mucous membranes have a bluish tint, and if the liver is damaged, they become jaundiced. Often, during a period of critical drop in temperature, vascular insufficiency develops: muscle tone drops sharply, peripheral veins become empty, visible mucous membranes turn pale, the temperature of the peripheral parts of the body decreases, the pulse becomes thread-like, heart sounds weaken, and blood pressure drops. During this period, conditioned reflexes disappear, reflexes of the skin and cornea decrease.
Animals have decreased appetite and slowed peristalsis. Gastritis and coprostasis are often observed. Diuresis in the first days of the disease is significantly reduced, and with the onset of the resolution stage it is noticeably increased. Accordingly, the physicochemical properties of urine change. In the first days of illness, urine has a high relative density (above 1.036), traces of protein are found in it, and the chloride content is reduced. In the resolution stage, the relative density of urine decreases, protein disappears, and the amount of chlorides increases. Urine reaction in herbivores in serious condition slightly acidic, and alkaline during the recovery period.
The morphological and biochemical composition of the blood changes: significant leukocytosis is noted, a nuclear shift to the left to young ones, rarely to myelocytes; the number of eosinophils decreases and the number of monocytes increases. ESR in the first days of the disease is slowed down, and in the resolution stage it is accelerated. The total amount of protein in the first three stages is increased to 8.5% due to an increase in the tlobulin fraction, the content of bilirubin also increases to 30 mg%, lactic acid - to 20 mg%; The chloride content and reserve alkalinity of the blood decrease. With the resolution of the process, the morphological and biochemical composition of the blood is restored.

Flow. The duration of the disease depends on the conditions of detention, feeding of the animals, the condition of the body, the timeliness and completeness of treatment. Timely treatment under good housing and feeding conditions often interrupts the process at the first stage of its development. In most cases, the disease lasts 14-15 days, and sometimes more. The latter happens when the disease is complicated by exudative pleurisy, hepatitis, in advanced cases- purulent pneumonia or gangrene of the lungs and ends in death.

The prognosis depends on the condition of the body, the location of the lesion and the duration of the course. More favorable for abortive forms of pneumonia, less favorable for lesions of the upper third of the lung and periaphragmatic area.

Pathological and anatomical changes. Each stage of development is accompanied by characteristic pathomorphological changes.
The flushing stage is characterized by hyperemia, blood stasis, slight exudation of serous fluid into the alveoli and interstitial spaces of the lung tissue. The affected lobe of the lung is slightly enlarged, dark red in color, rather dense; the lumen of the pulmonary alveoli, in addition to serous fluid, contains a small amount of red blood cells.
The stage of red liver is accompanied by further sweating of fluid, rich in protein and erythrocytes. The alveoli are completely filled with a coagulated red mass. The affected lobe of the lung is airless and resembles the liver in consistency and color.
In the stage of gray hepatization, fibrinous exudate contains a large number of leukocytes and rejected alveolar epithelium.
In the stage of yellow hepatization, the lung tissue is dense, yellow in color; in the lumen of the bronchi, a large amount of dense and a small amount of liquid mass of saffron-yellow color is found.
The resolution stage begins from the moment the inflammatory phenomena fade away. At this time, the alveoli are filled with yellow exudate; in some cases, growths of connective tissue (carnification) and death of the alveolar tissue are found.

Diagnosis. Diagnosis of lobar pneumonia is based on identifying its characteristic clinical signs. To them. include a rapid rise in body temperature, a constant type of fever, a large focus of dullness, bilateral nasal discharge of saffron-yellow color, and a staged process. At the same time, studies are carried out to diagnose atypical lobar pneumonia. In all cases of manifestation of lobar pneumonia, a thorough analysis of the epizootic situation and differentiation of lobar pneumonia from peripneumonia, bronchopneumonia, pleurisy and pericarditis is necessary.

Treatment. During treatment, the following tasks are set: to provide the sick animal with the necessary nutrients, reduce oxygen deficiency, delay the development of pathogenic microflora, create an outflow of blood from the affected part of the lung, normalize neurotrophic processes in these areas, promote the resorption and removal of accumulated exudate and eliminate symptoms indicating a critical condition of the body. To complete the assigned tasks, sick animals are placed in rooms with clean, dry and warm air. Mixed grass hay is included in the diet High Quality, malted and yeasted food, infusion of pine needles in small quantities. Warming compresses, warm wraps, mustard plasters, cupping, rubbing, skin, blocking nerve nodes and trunks with novocaine help to relieve the processes.
A. M. Kolesov (1945) proposed a treatment regimen for lobar pneumonia in horses, which can also be used for cattle. Treatment but its method depends on the stage of pneumonia: at the stage of hot flashes, rest is created, novarsenol is administered intravenously - 0.01 g per 1 kg of body weight (in isotonic sodium chloride solution), 10% calcium chloride solution - 200-250 ml, prescribed mustard plasters; in the stage of red and gray hepatization - novarsenol (second administration), mustard plasters or cups, rubbing the chest with irritating liniments, 20% camphor oil-20 ml 3 times a day or 10% caffeine - 20-30 ml subcutaneously, 400-600 ml 5% glucose solution into a vein and 0.5 units of insulin subcutaneously. per 1 kg of body weight; in the resolution stage, expectorants are given: ammonium chloride - 7-15 g, sodium hydrocaroonate - 20 g 3 times a day and diuretics: orally - juniper berries - 20-50 g, furosemide - 0.4, diacarb - 1.5-2, timisol - 5-10, hypothiazide - 0.25-0.5, potassium acetate (potassium acetate) - 25-60, bearberry leaves - 15-20, orthosiphon leaf - 30-35. hexamegalenetetramine (urotropine) orally and intravenously, 5-10 g 2 times a day for 3-4 days. Short walks are useful at this time.
Satisfactory results have been obtained from the use of norsulfazole, which is administered orally at a dose of 5-12 g (0.05 g per 1 kg of body weight) 4-5 times a day. Soluble norsulfazole ( sodium salt norsulfazole) is administered intravenously at 0.02-0.06 g per 1 kg of body weight 2-3 times a day for 4-5 days. in a row until body temperature drops. Good action sulfadimezine has an effect when administered orally after 4 hours at 0.08 g per 1 kg of body weight, on the 3-4th day of treatment - 0.02 after 6 hours, on the 5th day - but 0.01 g after 8 hours
Sulfonamide drugs are combined with antibiotics (penicillin, bicillin-3, streptomycin, terramycin) or broad-spectrum antibiotics are used (streptomycin, tetracycline, neomycin sulfate, erythromycin). When using antibiotics without prolongators, it is recommended to administer them 4-5 times a day for 4-6 days. until the main phenomena of the disease are eliminated, when using antibiotics with prolongators, they can be administered after 8-12-48-120 hours. It is useful to combine antibiotic therapy with novocaine blockade of the stellate ganglion - 0.25-0.5% solution of novocaine in a dose of 0.5 -1 ml per
1 kg of body weight or intravenous administration of a 0.5-1% solution of novocaine 30-50 ml for 2-3 days in a row, once a day, some recommend administering once every 3-4 days. Along with sulfonamides and antibiotics, mustard plasters, cupping, diathermy, and UHF are used. To accelerate the course of the disease, use calcium chloride or calcium glyconate. The pathogenetic effect is exerted by oxygen therapy and intravenous administration of glucose with ascorbic acid (0.5 ml of a 40% glucose solution and 7 mg of ascorbic acid) and subcutaneous insulin 0.5 units. per 1 kg of body weight. Oxygen is administered through a special mask or subcutaneously into the chest area in an amount of 10-12 liters. At the resolution stage, expectorants are prescribed: ammonium chloride - 7-15 g per day, if there is no intestinal catarrh, or sodium bicarbonate - 15-30 g.
Cardiac activity is supported with camphor. It is administered in oil solutions (20%) subcutaneously to large animals in a dose of 20 ml 2-3 times a day. Cordiamine is prescribed subcutaneously in 10-20 ml (25% solution). For vascular insufficiency, adrenaline (1:1000) - 1-5 ml is administered intravenously, norepinephrine (1:500-1:1000) - 2-5 ml in 100 ml of 5% glucose solution, mezaton, 1% - ny solution -
3 - 10 ml subcutaneously or intramuscularly. In prolonged cases, autohemotherapy is used - 30-50 ml daily for
4 - 5 days
At high body temperatures, antifibrin is given internally - 15-30 g, phenacytin - 15-25, latophenine - 10-15 g, a short-term cold shower is given, followed by rubbing the body, warm wrapping and keeping the patient in a room with an air temperature of about 20 ° C. If an animal has a severe cough, it is prescribed morphine subcutaneously, dionine - 0.2-0.3 g orally 1-2 times a day, omnopon - 0.2-0.3 g subcutaneously
2 times a day.

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 is 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 the involvement of the bronchi and respiratory tissue of the lung in the inflammatory process. 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 is complicated by 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.