Croupous pneumonia (pneumonia crouposa) is an acute disease characteristic of almost all types of farm animals.

As an independent process, lobar pneumonia occurs in contagious pleuropneumonia (horse), peripneumonia (cattle) and hemosptitsemia (small and large cattle, deer, pigs), as a complication - and also quite common - in swine fever, paratyphoid fever and some other diseases.

Lobar pneumonia affects all age groups, but it takes the most typical and striking forms in adult animals (see below for features of lobar pneumonia in young animals).

Pathoanatomically, lobar pneumonia is an acute exudative inflammation, characterized by the accumulation of fibrinous exudate in the airways (alveoli, bronchi), rapid involvement of large areas of the organ in the process - lobarity, etc. finally, unlike bronchopneumonia, it predominantly spreads through the lymphatic tract of the interstitium of the lungs, and not along the bronchial tree.

It is customary to distinguish the following stages of development of lobar pneumonia: rush of blood, red and gray hepatization and resolution.

The stage of influx, or flooding with blood, is expressed in a sharp hyperemia of blood vessels, especially respiratory capillaries. The alveolar lumens contain serous fluid, red blood cells and desquamated epithelium.

Macroscopically, the affected parts are slightly enlarged, dark red in color and have a moderately dense consistency. The cut surface is smooth and when pressed, bloody fluid is released. Pieces of lung immersed in water float heavily, but do not sink, which indicates the presence of air in the alveoli.

The stage of red hepatization is characterized by increasing diapedesis of erythrocytes and exudation of plasma proteins, in particular fibrinogen.

Upon microscopy, in addition to sharp hyperemia of the respiratory capillaries, a fibrin mesh of varying density, many red blood cells and a small number of polymorphonuclear leukocytes are found in the alveoli.

Macroscopically, the affected parts are sharply enlarged, dark red or red-brown in color, dense. Their cut surface is dry and indistinctly granular, since the exudate is relatively poor in fibrin. The granularity is caused by contraction of the elastic tissue of the lungs during the incision, as a result of which the fibrinous plugs of the alveoli protrude on the surface in the form of grains. In the stage of red hepatization, the lung tissue does not contain air, and pieces of it immersed in water drown.

The stage of gray hepatization is more extended in time. At this stage, there is a gradual discoloration of the affected parts, which first take on a gray-red color and then gray, which is explained, on the one hand, by the attenuation of hyperemia and diapedesis of erythrocytes, on the other, by increased fibrin deposition, cellular reactive processes (desquamation and proliferation of the alveolar epithelium) and emigration of leukocytes, which in the gray hepatization stage becomes widespread.

Macroscopically, as with red hepatization, the changed lobes are sharply enlarged, even more dense and dry, gray in color.

The development of the described stages of the process usually does not occur simultaneously in different parts of the lungs, which is why the cut surface of the altered lobes acquires a motley, marbled appearance, and the degree of marbling depends on the nature of the process: the more acute it is, the less pronounced the marbling, and vice versa.

The resolution stage is considered as a favorable outcome of lobar pneumonia, followed by regeneration. It is associated with the liquefaction and dissolution of fibrin by leukocyte enzymes; at the same time, the leukocytes themselves undergo obesity and decay and give the entire cut surface of the hepatized lung a gray-yellow color, which is why in such cases they also call gray-yellow hepatization.

Macroscopically, in the resolution stage, the affected lobes gradually lose their density. They become soft and flabby; when pressed, a cloudy, gray-yellow or reddish mass similar to pus separates from the cut surface.

Subsequently, liquid masses of exudate are removed by absorption through the lymphatic channels, partially by coughing through the bronchi, after which regeneration of the alveolar and bronchial epithelium occurs.

Fibrinous pneumonia most often affects the apical, middle and anterior - lower parts of the main lobes, from where the process can spread to a large part, and sometimes to the entire main lobe.

Lobar pneumonia of young animals has its own characteristics: these include:

the exudate is poor in fibrin, resulting in sluggish hepatization;

severe desquamation of the alveolar epithelium, so that the exudate is close to catarrhal in nature;

absence of a sign of lobarity (pneumonic foci are more like lobular ones).

In lobar pneumonia, as a rule, the interstitial tissue (interlobular, peribronchial) and pleura are affected. The interstitial tissue is found saturated with serous-fibrinous effusion, and its inflamed lymphatic vessels (lymphangitis) are sharply dilated and partially thrombosed.

Inflammation of the perivascular lymphatic sheaths can easily spread to the walls of blood vessels, which ultimately leads to widespread thrombosis of the latter.

Finally, the intimate contact of the lymphatic systems of the interstitial tissue of the lungs and the subpleura makes it clear that the pleura itself is involved in the pathological process. The latter is affected in the majority of cases of lobar pneumonia, so that practically the disease should be considered as pleuropneumonia.

Pleurisy usually occurs in the first stages of the disease and is limited to the area of ​​the hepatized lobes. Less commonly, they become more widespread and go beyond the specified limits (sometimes the pericardium and peritoneum are affected).

By nature, pleurisy refers to fibrinous or serous-fibrinous inflammation.

In the first case, the serous leaves are covered with dense and dry films or thick, compact masses of fibrin; in the second case, these films have a loose and spongy appearance of beaten egg white, and in the pleural cavities they find a turbid serous fluid with fibrin flakes suspended in it.

The further fate of the pleuritic exudate can be expressed in the fact that the enzymes of leukocytes dissolve fibrin, after which it is absorbed by the lymphatic pathways, while the serous cover regenerates. However, much more often, especially with massive deposits of exudate, an outcome is observed in the organization, with the formation of connective tissue growths on the pleura, and if both layers (visceral and parietal) are affected - connective tissue adhesions, initially tender and loose, later dense fibrous.

In addition, in some cases, purulent transformation of the exudate (pleural empyema) is noted.

The resolution of lobar pneumonia in animals is apparently rare: severe damage to the lymphatic vessels and their thrombosis exclude the possibility of resorption of the exudate. The outcome most often observed is carnification. Carnification is based on the process of organizing fibrinous exudate and replacing it with young, vascular-rich connective tissue. The affected parts of the lungs become dark red and resemble meat in color and consistency. Later, due to the transformation of granulation tissue into scar tissue, the affected lobes thicken and shrink, and their color turns from dark red to whitish.

Complications of lobar pneumonia include necrosis, gangrene and suppuration. Of these, necrosis serves as a necessary prerequisite for the occurrence of the other two. The origin of necrosis is associated with two points. In some cases, it is a consequence of the direct action of bacteria or their toxins on the liver tissue of the lungs. Such necrosis is delimited from living tissue by a jagged, gray-white demarcation line consisting of accumulations of polymorphonuclear leukocytes and their fragments. Later, granulation tissue and, finally, fibrous tissue develops around it (encapsulation).

In other cases, the appearance of necrosis is caused by vascular thrombosis; Such necrosis in its appearance resembles anemic infarctions and is especially common in peripneumonia of cattle.

Gangrene, as a complication of lobar pneumonia, develops due to the necrosis that preceded it, subject to the introduction of putrefactive microorganisms into the dead tissue. Gangrene especially often complicates contagious pleuropneumonia of horses. Long-term stasis, accompanied by significant diapedesis of erythrocytes (hemorrhagic accent of pneumonia), appears to have significant pathogenetic significance for the occurrence of gangrene.

Necrobiotic changes in hepatic tissue are also a prerequisite for the complication of lobar pneumonia by a purulent process. That is why necrotizing pneumonias are often abscess-forming.

Anatomical changes are expressed in the appearance of multiple yellow-green abscesses in the hepatized tissue. Sometimes individual small abscesses merge into one large one, but for the most part they remain isolated and subsequently become encysted.

Extrapulmonary processes in lobar pneumonia are poorly covered in the veterinary literature. There are only fragmentary indications regarding the degeneration of the kidneys, myocardium and liver. In the latter, blood stagnation and obesity are often found. In addition, cases of endocarditis have been reported, observed mainly in pneumonia complicated by sepsis.

In young animals, in addition to pericarditis, peritonitis sometimes occurs, especially with paratyphoid fever of calves and piglets.

Pathogenesis. There are still many unclear aspects in the pathogenesis of lobar pneumonia. Only the following points are more or less firmly established.

The process occurs in the form of single or multiple pneumonic foci.

It begins from the respiratory bronchi and spreads both peri- and endobronchially.

Peribronchial spread leads to inflammation of the lymphatic (lymphangitis) and blood vessels and their thrombosis.

The same principle of propagation causes the process to reach the pleura.

The endobronchial spread of the process contributes to the appearance of initially small acinous pneumonic foci, through the fusion of which and as a result of aspiration of masses of exudate, extensive pneumonia occurs.

The mechanism of formation of primary foci remains unclear. Some researchers defend their hematogenous nature, others (the majority) - aerogenic nature. There is no direct evidence in favor of the first or second route of infection yet. Some indirect considerations and, in particular, the fact of the simultaneous appearance of multiple primary foci and, moreover, in an area that has an isolated blood supply (acinus), rather indicate their hematogenous nature.

It is also not entirely clear why inflammation in lobar pneumonia relatively quickly takes on a lobar character. They try to explain the lobarity by the allergic nature of the process and the lymphogenicity of its spread. From this point of view, lobar pneumonia should be considered as a hyperergic inflammation of a sensitized organ, which is proven by relevant experiments, as well as by some inherent features of lobar pneumonia. These include: rapid coverage of a significant area of ​​the organ by the process, fibrinous and hemorrhagic exudate, indicating deep damage to the tissue and, in particular, the vascular wall.

Lobar pneumonia in certain animal species is described in the sections: “Peripneumonia of cattle,” “Contagious pleuropneumonia of horses,” “Hemorrhagic septicemia.”

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 farms for fattening 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 the allergic state of the 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 streams, or quickly transferring 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. The spread of the 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, fatty degeneration of fibrinous exudate and a further increase in the number of leukocytes occur.

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. In severe forms of the disease, if vigorous treatment is not carried out, death occurs due to 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, there is an improvement in the general condition of the animal, a decrease in body temperature, and normalization of 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 pronounced symptoms of lung damage, does not have a staged course of the disease and often becomes chronic.

Lobar pneumonia is an acute inflammation of the lower respiratory tract. It mainly affects horses and cattle, but can also occur in pets.

Causes
Typically, the disease occurs when a decrease in local and general immunity and the contamination of the lungs with pathogenic microorganisms coincide in time. As a rule, these are resistant strains of pneumococci, diplococci, and staphylococci. These types of bacteria are also found in healthy animals, but due to natural resistance to infectious diseases, they do not suffer from pneumonia.

In addition, pneumonia can be caused by a stressful situation that has caused the animal’s body to deplete all its reserves. For example, if you give cold water to a horse that is hot from running, or transport cattle from a warm room to a damp one. Another factor is hot or poisonous gas, which damages the bronchi and especially the lungs.

Clinic
They are practically no different from humans. The disease begins acutely: with weakness, lethargy, drowsiness caused by intoxication. The body temperature rises to febrile levels, the heartbeat becomes frequent, breathing becomes shallow, and the mucous membranes become sharply moist. There is a loss of appetite.

Specific symptoms include a dry barking cough, which gradually turns into a wet one. At this stage, you can hear fine wheezing in the lungs and crepitus. When tapping, tympanitis can be detected, then dullness of sound, and in the resolution stage - clear sound. Characteristics of lung percussion indicate the stage of the disease process. Depending on this, the unilateral or bilateral development of the pathological process is determined. To make it more likely, a chest x-ray is taken. In addition, sick animals experience purulent nasal discharge.

If the disease is detected on time and the animal is provided with the necessary medical care, then resolution of pneumonia occurs within a week to 10 days. Usually, after medical intervention, the disease becomes abortive in nature, and recovery occurs much earlier.

Sometimes the disease is prolonged due to the animal’s reduced immunity, resistance of the pathogen to drugs, or an atypical course of the disease. Its manifestations in this case can be very diverse, the duration varies from several weeks to months. Exacerbations and relapses are possible against the background of clinical recovery.

Diagnostics
To make a diagnosis of lobar pneumonia you must:
1. History, indicating the probable cause, symptoms of the disease and previous illnesses.
2. Laboratory tests:
- CBC (complete blood count), where we will see an accelerated ESR, an increase in leukocytes due to young neutrophils, and a decrease in lymphocytes.
- Fibrin, leukocytes, altered erythrocytes, and microbes are detected in nasal exudate.
- Having received a smear in the larynx and bronchoalveolar lavage, you can culture the cells that are the causative agent of the disease.
3. Instrumental research:
- X-ray: the image shows shadows in the lungs, usually in the lower lobes, which indicates an inflammatory process.
It is necessary to know the differences between lobar pneumonia and other diseases with similar symptoms. These are diseases such as swine flu, equine pleuropneumonia, rhinotracheitis and others.
It is difficult to make a prognosis for such a disease, especially if medical care is delayed for some reason.

Treatment
First of all, sick animals are isolated from healthy ones, and the room where they were kept is disinfected.
Sick animals change their diet, add more vitamins, proteins, fats, and provide animals with unlimited access to water.
Antibiotics that target typical pathogens are prescribed. But at the same time, a smear is taken for inoculation on a nutrient medium to check the susceptibility of the flora to the medicine. If necessary (lack of effect, deterioration of general condition), the antibiotic is changed. In parallel with this, local remedies are used, such as rubbing the animal’s chest with turpentine or mustard alcohol, antiallergic measures, and lowering the temperature (if necessary). Mucolytics and expectorants are good at accelerating the resolution of the inflammatory process. They remove accumulated exudate and prevent congestion in the lungs, which can prolong the disease.

If intoxication increases, then to maintain the body it is necessary to inject a hypertonic solution of glucose with vitamin C intravenously, and in order to prevent coma, insulin is injected at the same time.
In cases where maintenance therapy is necessary, for example, concomitant chronic heart or liver diseases, drugs are prescribed in therapeutic doses.

Prevention
It is necessary to observe a work and rest schedule, carefully monitor your pet’s area and, if necessary, supplement it with vitamins to strengthen the immune system. Regular vaccinations and examinations by a veterinarian will also be useful.

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 is often 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.