Lobar pneumonia in a horse. Pneumonia in animals

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, allergic factors, and suppression of the protective mechanisms of the respiratory system play a significant role in the development of the disease.

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

First stage - active hyperemia or hot flash - characterized by damming of the pulmonary capillaries with blood; the epithelium covering the alveoli swells and exfoliates, liquid exudate with an admixture of leukocytes and a large number of red blood cells accumulates in the alveoli. There is significantly less air in the affected area than in a healthy one, and by the end of the stage it is completely forced out of the alveoli. The high tide stage lasts from several hours to a day.
Second stage - red hepatization - lasts 2-3 days. At this stage, the alveoli continue to fill with exudate containing red blood cells and fibrinogen. Then the exudate coagulates, as a result of which the alveoli and bronchioles of the affected area are filled with coagulated fibrin with an abundant admixture of red blood cells, deflated epithelium and a small amount of leukocytes.
At the third stage - stage of gray hepatization - migration of leukocytes begins. The number of red blood cells gradually decreases, and the number of white blood cells increases. Under the influence of leukocyte enzymes, fibrin and other components of the exudate are destroyed and take on a gray color. The duration of this stage is 2-3 days.
Fourth stage - resolution stage - characterized by the fact that with an increase in the number of leukocytes, the exudate is broken down and liquefied and thus acquires the ability to be absorbed. The liquefaction of exudate is based on processes occurring under the influence of lipolytic and proteolytic enzymes of leukocytes. Under their influence, fibrin is converted into soluble albumose and amino acids (leucine, tyrosine, etc.). The liquefied exudate is partially absorbed and partially removed with sputum when coughing. Most of the absorbed exudate is excreted in the urine. Air gradually enters the alveoli that are freed from exudate, and at the same time regeneration of the alveolar epithelium occurs. The duration of the stage is from 2 to 5 days.
When opening animals that died from bronchopneumonia, inflammatory foci of various sizes are found in the lungs, colored red-brown, gray-red or gray-white, rising above the surface of the lung. The bronchi contain mucous or mucopurulent exudate. In the chronic course, fibrous fusion of the pulmonary pleura with the costal pleura, and often with the pericardium, is found;
Pathological changes for lobar pneumonia depend on the stage of development of the disease. At the stage of tide, the lung is full of blood and increased in size. The cut surface is smooth and shiny. At the stage of red hepatization, the affected part of the lung is without air, enlarged, resembles a liver in section, and sinks in water. The cut surface is red, granular, due to the fact that the alveoli are filled with coagulated fibrinous exudate and protrude above the cut surface. At the stage of gray hepatization, the lung initially has a gray tint, and at the resolution stage it becomes yellowish. Along with the above-described stage changes, one can detect an increase in bronchial lymph nodes and degeneration of parenchymal organs. At the resolution stage, the lung resembles the spleen in consistency.
Symptoms in acute alveolar emphysema, they manifest themselves as severe shortness of breath, a horn-shaped dilatation of the nostrils when inhaling and protrusion of the anus when exhaling. During auscultation, weakened vesicular breathing is heard, and if the cause of emphysema is bronchitis, wheezing is detected. The posterior border of the lungs is pushed back 1-2 ribs, the percussion sound is boxy.
In chronic alveolar emphysema, expiratory dyspnea is well expressed, exhalation is biphasic. The chest is barrel-shaped. When exhaling, retraction of the intercostal spaces is noted, and an ignition groove is formed along the costal arch. With auscultation, depending on the origin of emphysema, wheezing or weakening of vesicular breathing is detected, and with percussion, an increase in the boundaries of the lungs and a boxy percussion sound.
Interstitial emphysema is acute and develops quickly. Characterized by rapidly increasing shortness of breath and increased heart rate. On auscultation, weakened vesicular breathing and crepitating rales are heard. When air penetrates under the skin, a crepitation noise is detected.
Hematological examination in horses can reveal an increase in the number of red blood cells and hemoglobin.
The first symptoms of bronchopneumonia are characterized by depression of the animal, general weakness, body temperature usually rises by 1-2 °C, and scant serous-mucosal or mucopurulent discharge is observed from the nasal cavities. Shortness of breath is usually 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. A typical symptom of 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. The dullness can be of different sizes, its borders have different shapes, but the upper border is always arched upward. At the resolution stage, the percussion sound acquires a tympanic hue, and as the normal state of the lung tissue is restored, it becomes clear, atympanic.
During auscultation at the stage of hyperemia, increased vesicular breathing is initially detected, and by the end of the stage, crepitating fine bubbling rales are heard during the inhalation phase. With the development of the hepatization stage, wheezing disappears, a gradual disappearance of vesicular breathing and the appearance of bronchial breathing are established, sometimes respiratory sounds in the lesion are not audible at all. At the resolution stage, rough, moist rales are heard, which become more and more numerous and drown out bronchial breathing. Then the sonority of wheezing gradually decreases, bronchial breathing weakens and turns into normal vesicular noise.
A characteristic symptom of lobar pneumonia is the appearance of saffron-yellow or rusty-brown nasal discharge at the stage of hepatization. It is observed before the resolution stage begins.
Certain changes in lobar pneumonia are observed in the activity of the cardiovascular system. From the very beginning of the disease, the pulse is increased, but this increase is not proportional to the increase in body temperature (the temperature rises by 3-4 ° C, and the pulse increases by 10-15 beats). This discrepancy is typical for 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 also 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 data from anamnesis, clinical manifestations, and laboratory tests. Infectious and invasive diseases occurring with respiratory syndrome, as well as lobar pneumonia and other lobular pneumonia 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 (persistent fever, saffron yellow fibrinous discharge from the nasal cavities, stages of disease development, damage to the entire lobe of the lung with the superior arcuate line), and laboratory blood tests. In the differential diagnosis, infectious diseases such as contagious pleuropneumonia of horses, peripneumonia of cattle, 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.
The highest effectiveness in the treatment of animals with bronchopneumonia is obtained with timely initiation of complex therapy for patients with acute disease. 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 pulmonary congestion, it is recommended to carry out bloodletting (in horses 2-3 l), antibiotics and sulfonamides are used as antibacterial agents. 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 are used (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. For symptomatic therapy, they use cardiac, expectorants, 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 use and especially timely and complete treatment of 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).

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1. Protocol№ 1

02/6/2013 Oryol Veterinary and Sanitary Plant

Autopsy of the corpse of a bull calf, aged 2 months, black-and-white breed, owned by CJSC AIC “Orlovskaya Niva” JV Saburovo.

The autopsy was performed in the section hall of the veterinary and sanitary plant by B.L. Belkin, professor of the department of anatomy and physiology of farm animals. February 6, 2013 in the presence of 4th year students of the Oryol State Agrarian University.

Anamnestic and clinical data are unknown.

External inspection.

1) The corpse of a bull of a black and white breed, black and white, of average fatness, regular physique, weighing about 65 kg.

2) The eyes are not tightly closed, the eyelids are without visible damage, the eyeball is slightly sunken, the cornea is transparent. The conjunctiva is pale red and smooth. The pupil is dilated. The ear canals are clean. The condition of the nasal passages, the circumference of the nostrils and the shape of the nose are anatomically correct. The anus is closed, not dirty, and there is no discharge.

3) The skin is dry, elastic. The coat is thick, of moderate length, smooth, and adheres well to the skin. The subcutaneous tissue is devoid of fatty deposits, there are no hemorrhages, and there are cadaveric spots on the left side.

4) The volume of skeletal muscles is slightly reduced, the macular muscles practically do not protrude. The consistency of the muscles is elastic, the color is dark red, the pattern of the fibrous structure is pronounced.

5) The bones are hard, the movable joints are not deformed. The articular surfaces of the bones are smooth, shiny, and white. The tendons are not damaged, strong, white.

6) Rigor mortis in the skeletal muscles is weakly expressed, on the left side there are small rigor spots in the subcutaneous tissue. There is no cadaveric decomposition.

Internal inspection.

7) The abdominal cavity contains a small amount of clear fluid. Position of the abdominal organs: anatomically correct. The serous covers are white, smooth, dull, and moist.

8) The position of the thoracic cavity organs is anatomically correct. There is no fluid in the chest.

Blood, hematopoietic and immune organs.

9) There is no blood supply to the internal organs. Blood that has not coagulated is reddish-dark in color.

10) Lymph nodes: superficial (submandibular, prescapular, patellar, external inguinal) - oval in shape, flabby consistency, slightly enlarged, no blood supply, gray-red in color when cut, juicy; mesenteric and internal inguinal lymph nodes: not enlarged, without edema, gray color on section.

11) The spleen is not enlarged in volume, the edges are sharp, of a softish consistency, the capsule is not tense, brown-red in color, the edges converge on the cut, tissue scraping is insignificant.

12) Bone marrow is dark red in color, moderately juicy, and has a jelly-like consistency.

13) The tonsils are enlarged and reddish in color.

Cordially - vascular system.

14) The heart sac contains a small amount of clear liquid. The serous membrane is smooth, shiny, pale gray in color.

15) The heart is round - oval in shape, the apex of the heart is blunt, the ventricles are filled with well-coagulated blood, the patency of the valves is preserved. The valves are shiny, smooth, the semilunar valves are thin, transparent; the myocardium is gray-red in color, flabby consistency, the endocardium is smooth and shiny. There is no epicardial fat.

16) The aorta and pulmonary artery are elastic, the inner membrane is gray-white, smooth, shiny.

Respiratory system.

17) Nasal cavity: contains a significant amount of mucus, the mucous membrane is dark pink, reddened in places, swollen.

18) Larynx, trachea, bronchi: cartilages are intact, the contents are a small amount of mucus, the mucous membrane is moist, smooth, shiny, pale pink. There are also streaky hemorrhages and foamy fluid on the larynx.

19) The marbling of the lung is clearly expressed, the costal and pulmonary pleura are fused, fibrin overlays are clearly visible. The cranial part of the right lung has a dense consistency. There is no fluid in the lungs.

Digestive organs.

20) The oral cavity is slightly open, the bite is correct, the tongue is bitten, the mucous membrane is pale pink and moist. Pharynx: the mucous membrane is pinkish in color, the folding is pronounced, there is no content, the mucus is insignificant. Esophagus: the mucous membrane is pinkish in color, smooth, shiny, moist, pronounced folding, no contents, little mucus.

21) Stomach: tripe contains curdled casein clots and a significant amount of mucus; the mesh and book are empty, contain a small amount of turbid liquid, the mucous membranes of the proventriculus are gray-green in color, easily peel off from the submucosal layer; the abomasum is significantly filled with milk clots and dirty gray liquid, the mucous membrane is reddened in places with hemorrhages. Throughout the mucous membrane and in the contents of the abomasum there is a large amount of turbid, viscous mucus.

22) In the small intestine there is a small amount of feed masses of gray-green color. The mucous membrane is pale, covered with mucus. In the large intestine, the cecum and colon are filled with a liquid, mushy mass, the mucous membrane is pale red, there is little mucus; in the rectum, the feces are mushy, greenish in color, the mucous membrane is pale gray.

23) Liver: the gallbladder is filled with bile, the patency of the bile duct is preserved, the bile is thick, viscous yellow-green in color. The liver is not enlarged, has a soft consistency, is evenly colored, dark blood flows down the cut, the lobulation is smoothed, the tissue scraping is significant.

24) Pancreas: elastic consistency, gray-pink color with a well-defined lobular structure.

Urogenital organs.

25) Kidneys: the fat capsule is moderately expressed, its own capsule is easily removed. The kidneys are slightly enlarged, soft in consistency, brown in color, the edges of the cut converge, the cut surface is smooth, on the cut the border of the cortical and medulla layers is smoothed, the scraping is significant, tissue. The mucous membrane of the renal pelvis and ureters is gray-red in color.

26) Bladder: not full of urine, light yellow in color, cloudy, with an admixture of grayish-white flakes in a small amount; the mucous membrane is gray-pink in color.

27) The genitals are developed according to age.

Pathological diagnosis:

1) Lobar pneumonia

2) Dilatation of the right ventricle

3) Granular kidney dystrophy

4) Acute catarrhal rhinitis

Lobar pneumonia

Lobar pneumonia(Pneumoniacrouposa) - acute inflammation of the lungs, characterized by high fever and profuse sweating of fibrinous exudate into the alveoli and bronchioles. The disease is observed in all types of farm animals. More often recorded in horses.

Etiology

Weakening of the body under unsatisfactory feeding and maintenance conditions and thereby creating favorable conditions for the pathogenic effects of various microorganisms (pneumococci, etc.), allergic reactions. Stages of lobar pneumonia: flush (inflammatory hyperemia), red hepatization, gray hepatization, resolution.

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 along the lymphatic pathways 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 resolution stage. In the stage of hyperemia, a strong dilation of blood vessels occurs and they overflow with blood into the epithelium of the alveoli. Viscous exudate, leukocytes and red blood cells 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 are stopped. 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 at the stage of a rush of blood, sounds are heard in the affected areas, mainly in the lower third, less often in the middle third of the chest. crepitus and harsh vesicular breathing. 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 in the cardiovascular system occur from the first days of the disease. 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. The urine reaction of herbivores in severe condition is slightly acidic, and during the recovery period it is alkaline.

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 globulin 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 near the diaphragmatic area.

Pathological 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; in the lumen of the pulmonary alveoli, in addition to serous fluid, there is a small amount of red blood cells. The red liver stage is accompanied by further sweating of fluid rich in protein and red blood cells. 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 gray 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

corpse calf lobar pneumonia

Diagnosis of lobar pneumonia is based on identifying its characteristic clinical signs. These include a rapid rise in body temperature, a constant type of fever, a large focus of dullness, bilateral nasal discharge of a 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 objectives 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, talking about a critical condition of the body. To complete the assigned tasks, sick animals are placed in rooms with clean, dry and warm air. The diet includes high-quality forb hay, complexed and yeasted feed, and pine needle infusion 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 according to his method depends on the stage of pneumonia: at the stage of influx, 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, in vein 5% glucose solution - 400-600 ml and subcutaneous insulin 0.5 units. 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 of 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 subsides. Sulfadimezin has a good 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 d 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 symptoms 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 0.5-1% solution of novocaine 30-50 ml 2-3 days in a row once a day, some recommend administering it 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 gluconate. 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). In case of 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% - 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 - orally 0.2-0.3 g 1-2 times a day, omnopon - subcutaneously 0.2-0.3 g 2 times a day.

Prevention

Hypothermia, overwork, overcrowding, and strong exposure to irritating substances on the respiratory tract should not be allowed. Make sure that the diet includes the necessary nutrients and catalysts, avoid strong stimulation of the nervous system, oversaturation of the air with microflora and saprophytes, and rapid mixing of young animals from different farms.

Bibliography

1. Belkin B.L. Pathoanatomical diagnosis of animal diseases (with the basics of forensic veterinary examination) / B.L. Belkin, V.S. Prudnikov. - 2nd ed., add. - Orel: Orel State Agrarian University Publishing House, 2012. - 388 p.

2. Zharov A.V. Pathological anatomy of farm animals / A.V. Zharov - ed. reworked and additional - M.: Kolos, 2006. - 667 p.

3. Zharov A.V. Forensic veterinary medicine / A.V. Zharov. - M.: Kolos, 2001. - 264 p.

4. Kokurichev P.I. Fundamentals of forensic veterinary examination / P.I. Krkurichev, M.A. Dobin. - M.: Kolos - 264 p.

5. Salimov V.A. Workshop on pathological anatomy of animals / V.A. Salimov. - M.: Kolos, 2003 - 189 p., ill.

6. Shcherbakov G.G. Internal diseases of animals / G.G. Shcherbakov, A.V. Korobov. - St. Petersburg: Lan Publishing House, 2002. - 736 p.

7. Handbook of diseases of farm animals / D.D. Butyanov [and others]. - 2nd ed., revised. and additional - M.: Harvest, 1990. - 352 p.

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The disease is characterized by purulent inflammation of the lungs as a result of the introduction (metastasis) of purulent origin from other pathological foci of the body. Involvement of the lungs in the pathological process can be in the form of disseminated (point) lesions and abscess.

Etiology. Basically, this is a secondary disease that occurs as a complication of septic processes of various origins: pyosepticemia, purulent inflammation of the uterus, pharyngitis, ulcerative endocarditis, ulcers, purulent wounds, abscesses, surgical interventions.

Pathogenesis. In all cases, pyemic emboli clog certain blood vessels of the lungs with the formation of hemorrhagic infarctions and pyemic nodules (metastatic form), from which necrotic foci can appear in the lung tissue, and from their fusion large lesions are formed (lung abscess).

This is usually accompanied by the development of sepsis, varying degrees (usually severe) weakness of the cardiovascular system, loss of strength and frequent death of animals from general sepsis.

Symptoms The most typical symptoms are shortness of breath, painful cough, and refusal to feed. Subsequently, with the development of abscesses in the lungs, the animal’s condition sharply worsens, fever intensifies to 40-41°C, characterized by daily fluctuations in body temperature and sweating in most animals.

Auscultation reveals weakening of respiratory sounds, wheezing, bronchial or amphoric breathing. In cases of rupture of the abscess, the animal’s condition usually improves somewhat, and purulent or mucopurulent fluid, often foul-smelling, flows from the nose. It contains elastic fibers and particles of lung tissue. There are signs of pleurisy.

In the presence of small lesions, percussion does not establish deviations from the norm, but in the case of large lesions (abscesses), dullness or a nearby tympanic sound is observed, indicating the development of vicarious emphysema. When a large abscess ruptures and empties, the percussion sound may have a metallic tint. With complications in the pleura, auscultation may produce pleural friction sounds, and percussion may be painful.

Pathomorphological changes. Single or multiple abscesses are found in the lungs, mostly superficial, ranging in size from a pea to a walnut, the inner surface of which is villous, the surrounding tissue is compacted and does not contain air. Entire lobes of the lung are often hepatized, the cut surface of which is dotted with small grayish-yellow spots. Over time, they can be encapsulated in a connective tissue membrane with a curdled mass inside. The pleura in places of superficially located foci is affected by serous-fibrinous or purulent inflammation.

Diagnosis. The presence of a purulent process in the lungs* in most cases can only be assumed. It can be confused with chronic pneumonia, purulent pleurisy and other lung diseases, which themselves may be secondary.

X-ray examination has the most important diagnostic value, although for the final diagnosis of the disease all of the given clinical symptoms and the course of the disease should be taken into account.

In differential diagnostic terms, other diseases of the respiratory system should be excluded on the basis of their characteristic clinical manifestations and special research methods.

Forecast. With the development of general sepsis and collapse - unfavorable. In other cases - doubtful. If it is possible to eliminate the underlying disease, the prognosis may be favorable.

Treatment. Sick animals need good maintenance; they are prescribed anti-streptococcal serum, auto-hemotherapy, immune drugs, ASD-2, subcutaneous hydrolysates, antibiotics and sulfonamide drugs are administered orally. Heat in all forms and cardiac medications are indicated on the chest.

Prevention follows from the etiology and consists mainly of preventing lung diseases and timely treatment of sick animals.

A febrile disease characterized by fibrinous inflammation of the lungs of the lobar type. Mostly horses are affected.

E T I O L O G Y

The primary role in the occurrence of lobar pneumonia is given to two factors: pathogenic microflora and the allergic state of the body.

Most researchers associate the occurrence of lobar pneumonia with an increase in the body's allergic reaction caused by a strong irritant - a stressor.

P a t o g e n e s

The pathological process in lobar pneumonia in most cases develops rapidly (hyperergic inflammation) and is characterized by the rapid coverage of large areas of the lungs within several hours and the leakage of hemorrhagic-fibrinous exudate into the cavity of the alveoli. The inflammatory process in the lungs as a result of the penetration of pathogenic microflora spreads in three ways: bronchogenic, hematogenous and lymphatic.

The typical course of lobar pneumonia is characterized by a certain staged development of the inflammatory process.

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 cellular capillaries with blood, the patency of the capillary walls is impaired, diapedesis of erythrocytes, sweating of serous-hemorrhagic exudate into the lumen of the alveoli and bronchi, and swelling of the alveolar epithelium.

The stage of red hepatization is characterized by filling the lumen of the alveoli and bronchi with coagulated substances from erythrocytes and plasma proteins, mainly fibrinogen. The duration of this 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 occurs and the number of leukocytes in it further increases.

The resolution stage is characterized by liquefaction of fibrinous exudate under the action of proteolytic and lipolytic enzymes, ero resorption and partial release through the respiratory tract during coughing. The duration of the permit station ranges from 2-5 days.

With lobar pneumonia, the function of the central nervous system, heart, liver, kidneys, intestines and other organs is impaired.

Pathological changes

In the stage of inflammatory hyperemia, the affected areas of the lungs are enlarged in volume, swollen, red-blue in color, do not sink in water, and when pressed, a foamy reddish liquid is released from the lumen of the bronchi when cut.

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), graininess is expressed on the cut, and they sink in water. In the stage of red hepatization, the coagulated fibrous 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 and migration of leukocytes.

In the resolution stage, the lung resembles the spleen in consistency and color, the granularity is less pronounced.

Symptoms

In typical cases, lobar pneumonia occurs acutely, less often subacutely.

Signs of the disease appear suddenly: in sick animals, general depression quickly increases, appetite is lost, breathing becomes sharply rapid and tense, hyperemia and yellowness of the mucous membranes appear. Fever of a constant type: from the first day of illness with a typical staged development and until the stage of resolution, it remains at a high level regardless of the time of day, in a horse it is usually within 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.

In the first hours and days of illness, a dry, painful cough is noted, which later becomes less painful, dull and wet. The stage of red hepatization is characterized by bilateral outflow of brown or reddish-brown hemorrhagic-fibrinous exudate from the nasal openings. Upon auscultation in the stages of inflammatory hyperemia and resolution, harsh vesicular or bronchial breathing, crepitus, and moist rales are detected.

In the stages of red and gray hepatization, dry rales, bronchial breathing are listened to, or the absence of respiratory sounds in the areas of hepatization is detected. Percussion in the stages of inflammatory hyperemia and resolution in places of lung damage reveals a sound with a tympanic tint, and in the stage of hepatization - areas of dullness or dullness with a border that is arched and convex and located in the upper third of the pulmonary field.

D i a g n o z

based on anamnesis and clinical symptoms, the main of which are: suddenness of the disease, acute course, constant type of fever, staged course, extensive zone of dullness of the lung area in the form of an upward curved arc - corresponds to the upper arcuate line of the lung.

A blood test reveals leukocytosis with an increase in the number of band neutrophils and the presence of young neutrophils, lymphopenia, eosinopenia, a sharply increased ESR, a relative increase in globulin and a decrease in albumin protein fractions, the presence of a large amount of fibrin and direct bilirubin in the plasma.

X-ray examination reveals extensive intense foci of darkening of the pulmonary field. The intensity of the darkening is most pronounced in the stages of red and gray hepatization.

PROGNOZ

Cautious, delaying the provision of medical care is often unfavorable.

Treatment

The main goal of drug treatment is to influence pathogenic bacterial microflora, aimed at its destruction.

Etiotropic bacterial therapy is carried out immediately after diagnosis, for which antibiotics or sulfonamide drugs are used in maximum doses.

Antibiotics and sulfonamide drugs are prescribed for a course of treatment in such a way as to ensure their constant therapeutic concentration in the blood.

Antibiotics are administered intramuscularly 3-4 times a day for 6-10 days in a row at an average rate of 7000-10,000 units/kg. If antibiotics do not provide an effect, it is advisable to use other antibiotics in maximum therapeutic doses (preliminary laboratory testing determines the most active antibacterial drug and the sensitivity of the pulmonary microflora to it).

Norsulfazole, sulfadimezin, etazol or sulfonamide drugs of similar dosage are given orally 3-4 times a day for 7-10 days in a row.

In parallel with antibacterial therapy, pathogenetic, replacement and symptomatic therapy is indicated.

Antiallergic drugs include intravenous injections of sodium thiosulfate and calcium chloride. For this purpose, you can also use suprastin or pipolfen internally.

With progressive intoxication of the body, hypertonic solutions of glucose with ascorbic acid, sodium chloride or hexamethylenetetramine are administered intravenously.

When symptoms of cardiovascular failure develop, caffeine, intravenous camphor-alcohol solutions, strophanthin, cordiamine, adrenaline are used in therapeutic doses, and in case of hypoxia, oxygen therapy is carried out.

To accelerate the resorption of exudate at the resolution stage, expectorants and diuretics are used in a complex of therapeutic agents.

In the first 3-4 days of illness, in parallel with antibacterial drugs, they recommend: unilateral blockade of the lower cervical sympathetic nodes, rubbing the chest walls with turpentine or 5% mustard alcohol, calves and small animals placing jars on the lateral surfaces of the chest wall, using inductothermy, UHF, heating the chest with incandescent lamps (not in the heart area), warm wraps, heating pads and other means of physiotherapy.

In cases of a sluggish or chronic course, with slow resorption of pneumonic foci, pneumosclerosis and the transition of inflammation to the pleura, autohemotherapy, iodine preparations, ion therapy, etc. are indicated.

P r o f i l a c t i c a

Aimed at increasing the body's resistance, compliance with maintenance technology and proper use of sports and working animals.

Lobar pneumonia(Pneumonia crouposa)

Lobar pneumonia- acute, cyclically developing inflammation of the 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 in the cardiovascular system occur from the first days of the disease. 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. The urine reaction of herbivores in severe condition is slightly acidic, and during the recovery period it is alkaline.
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.

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 red liver stage is accompanied by further sweating of fluid rich in protein and red blood cells. 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 objectives 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 critical condition of the body. To complete the assigned tasks, sick animals are placed in rooms with clean, dry and warm air. The diet includes high-quality forb hay, malted and yeasted feed, and pine needle infusion 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, in vein 5% glucose solution - 400-600 ml and subcutaneous insulin 0.5 units. 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 of 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. Sulfadimezin has a good 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 d 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.