Общая патологическая анатомия животных = Introduction to the pathological anatomy of animals. Учебно-методическое пособие

Alteration leads to a powerful release of biologically active substances – mediators of inflammation. The process of release of inflammatory mediators is a trigger of inflammatory reaction. The main source of inflammatory mediators are labrocytes (mast cells), macrophages, tissue basophils and other leukocytes. The cytoplasm of these cells is filled with granules, which are BAS-mediators of inflammation. When these cells are destroyed, histamine, serotonin, heparin, prostaglandins and others are released. They affect primarily on the vascular walls of the microcirculatory bed, which causes the development of vascular reaction-exudation and emigration.

Exudation quickly follows the alteration and release of mediators. It is exudation that plays a huge role in the deployment of the entire complex of tissue changes in inflammation. In the process of exudation we distinguish:

1.The reaction of the microcirculatory bloodstream with a violation of the rheological properties of the blood.

2.Manifestation of increased vascular permeability at the level of microcirculatory bed.

3.Exudation-the output of the liquid part of the blood outside the vessel

4.Emigration of blood cells, primarily leukocytes.

The reaction of the microcirculatory bloodstream is the most striking morphological sign of inflammation. Changes in the vessels of the inflamed area begin under the action of histamine with a reflex spasm of the microvessels. Lumen of arterioles, precapillaries, capillaries decreases. There is a spasm of the vessels of the microcirculatory bloodstream. Arterial hyperemia develops. But, a little later, there is a relaxation of blood vessels, there is an expansion of their lumen, especially in venules and the overflow of these blood vessels. Venous hyperemia in the focus of inflammation develops. Then stasis develops. Regional standing of leukocytes is observed (marginalia).

Increased vascular permeability – observed at the level of the microcirculatory bed. It is one of the most significant signs of inflammation, as the whole range of tissue changes, the originality of different forms of inflammation is determined by the degree of vascular permeability. Increased permeability is determined by venous

51

stagnation and the accumulation of acidic metabolic products. The third and fourth phases of exudation – exudation itself and emigration – are associated with increased vascular permeability.

Exudation and emigration. First of all, the liquid part of the blood, that is, liquid (water) and plasma proteins, go beyond the vascular wall. This forms a liquid exudate. As the vascular permeability increases, blood cells go beyond the vascular wall – emigration develops and more dense types of exudate are formed. Along with these processes the so-called cellular infiltrate will be formed, which consists of cells of conditionally hematogenous and histogenic (tissue) origin.

Proliferation or reproduction in the focus of cell inflammation is a kind of the final stage of inflammation, when there is a limitation of the focus of inflammation from the surrounding relatively healthy tissue.

Feature: proliferation in the focus of inflammation is observed throughout the inflammatory reaction, but this process can be expressed in different ways. Mesenchymal, tissue, adventitial, reticular endothelial cells propagate, as well as T- and B-lymphocytes, monocytes multiply in the inflammation. The above mentioned cells (especially the immature) can differentiate into various cells, but most often they differentiate in the elements of CT, for example, differentiated mesenchymal tissue cells are transformed into epithelioid cells. Histiocytes, macrophages, B-lymphocytes are converted into plasma cells or plasma cells. Monocytes turn into macrophages. As a result, all these round cell elements form a mature fibrous CT, which will limit the inflammatory focus from the surrounding tissue.

Morphogenesis of inflammatory reaction

1.At first, water and small protein molecules (albumin) enter the inflammation site, liquid exudate, for example serous, is formed.

2.Then the molecules of a larger protein – fibrinogen, which turns into fibrin, form a denser fibrinous exudate, enter the focus of inflammation.

3.In the focus of inflammation leukocytes rush (micro - and macrophages, lymphocytes and other cells). They give even more dense types of exudate-purulent exudate.

4.When exposed to coarse phlogogenic agents in the focus of inflammation cells that do not have chemotaxis begin to leave, hemorrhagic exudate is formed.

52

5. With blood in the focus of inflammation enters the mass of nutrients, which has a beneficial effect on the reproduction of CT. Here fibroblasts, fibrocytes, histiocytes multiply, and form a fibrous CT and immure the focus of inflammation.

Classification of inflammation

I. By manifestation: acute and chronic.

II. By the manifestation and participation of the immunocompetent system:

hyperergic, hypoergic and normergic.

III. By the prevalence of one or another component of inflammation over another:

1. Alterative: cell damage prevails in the focus of inflammation.

a) acute – in the focus of inflammation necrosis and degeneration dominate

b) chronic – atrophy prevails.

2. Exudative (the most capacious type of inflammation)

(a) serous: liquid exudate prevails.

-serous inflammatory edema,

-serous-inflammatory hydrocele,

-bullous inflammation.

b)fibrinous: in the focus of inflammation exudate with an admixture of fibrin protein accumulates

- croupous (surface), - diphtheritic (deep)

c)purulent: with the formation of a thick cream or cream - like exudate (pus).

- abscess: cavity filled with pus

- phlegmon: diffuse purulent inflammation in the loose tissue - empyema: purulent inflammation of natural cavities.

d)hemorrhagic: blood is observed in the exudate.

e)ihoroscope (putrid, gangrenous): putrefactive microflora joins.

f)catarrhal: inflammation of the mucous membranes. Can be any, except of fibrinous.

3. Proliferative:

a)interstitial inflammation (daily)

b)granulomatous

c)inflammation around foreign objects

53

d)inflammation around the helminths and their larvae

e)inflammation with formation of polyps and warts

f)hyperplastic inflammation in lymphoid tissue

Terminology of inflammation

Designation of inflamed tissue or organ is formed by adding to the root of the name of the tissue or organ in Latin transcription – "-itis".

To indicate a more accurate place of inflammation development, prefixes are used indicating a certain part of the body:

"couple" ("para") - about, near, around (prehepatic, periarteriit etc.) "peri" ("peri") - inflammation of the private shell body (perihepatic) "meso" ("meso") - inflammation of middle layers of body

(mesoarteritis)

"endo" ("endo") indicates the internal layers of the organ, for example, endocarditis.

With the exception of inflammation of the lungs – pneumonia, inflammation of the pharynx and peripharyngeal lymphoid ring -angina.

Characteristics of individual forms of inflammation Alterative type of inflammation (parenchymal inflammation)

This is an inflammatory process characterized by the predominance of dystrophic, necrotic and atrophic changes in the focus of inflammation with less pronounced exudative and proliferative changes. Most commonly develops in the parenchymal organs. The causes are viral and bacterial infections, as well as exposure to strong phlogogenic agents.

Morphology: depends on the course, that is, acute or chronic form.

Alterative inflammation in acute course occurs with pronounced necrosis, granular, fat and more severe forms of dystrophy. From mucous membranes epithelium is selected, foci of necrosis are formed in the tissues. Exudative phenomena are weakly expressed, hyperemia, a weak exit beyond the vascular wall of the liquid part of the blood, a slight proliferation of cellular elements are noted (more than organ stroma).

Examples:

1. acute myositis and myocarditis in malignant foot and mouth disease. Macroscopically, the myocardium resembles a drawing of a tiger skin - "tiger heart", due to the alternation of areas of venous

54

hyperemia with individual bundles of gray-white or gray-yellow in a state of granular, fat dystrophy or necrobiosis.

2. caseous pneumonia in tuberculosis: the focus of the alteria in the form of a focus of caseous (curd) dry necrosis of gray-white or grayyellow color, around which there is a hyperemic zone of borderline inflammation.

Chronic alterative inflammation is characterized by atrophic changes in the focus of inflammation. Develops owing to the impact on the cloth with a mild, but chronic flowing of stimuli: feed intoxication diseases.

Morphologically, the body is reduced in volume, the edges of the organ are thinned (for example, in the liver, spleen), the organ is dense to the touch, the body shrinks from the surface, acquires a shagreen appearance. The color is pale (due to ischemia), the incision reveals a growth of CT.

Clinical significance: in acute inflammation there is a sharp change in the functioning of the inflamed organ, perhaps even the death of the animal in inflammation of vital organs. Chronic alterative inflammation is characterized by a sharp decrease in the functional ability of the inflamed organ.

Exudative type of inflammation

It is characterized by the predominance of the second (exudative) phase of inflammation, when vascular phenomena prevail, vascular hyperemia is expressed, beyond the vessel of the components of the blood. With exudative inflammation, alterative phenomena are present, but they are in the background. Under the action of a weak stimulus, the liquid part of the blood rushes outside the vessel wall: water, mineral salts, albumins, globulins. Serous exudate is formed. When stronger stimuli appear plasma with the fibrinogen goes outside the blood – fibrinous exudates forms. With the influence of stronger stimuli emigration of shaped elements with the formation of purulent and hemorrhagic exudates begins.

Feature: types of inflammation pass into each other or combine.

Serous inflammation

This is the mild kind of exudative inflammation, characterized by the formation of liquid exudate containing 2-3% protein, isolated

55

polymorphonuclear leukocytes (PNL) and squamosed epithelial cells. Serous inflammation develops most often in serous cavities, mucous membranes, soft brain membranes, skin, and less often – in internal organs.

Etiology: weak infectious agents, thermal and physical factors, autointoxication. The development of serous inflammation in the skin is associated with exposure to specific viruses from the Herpesviridae family (smallpox, herpes, etc.).)

Morphology: inflammation accumulates turbid or opalescent liquid, poor in cellular elements, which are dominated by polymorphonuclear leukocytes and descended epithelial cells.

Depending on the localization we can allocate:

1.Sero-inflammatory edema: accumulation of exudate in the tissue between the tissue elements, usually in loose CT, for example, in the subcutaneous, intermuscular tissue, stroma of parenchymal organs.

Macroscopically, there is swelling, thickening of the stroma of the body, the body becomes a cramped consistency, with an acute process, the surface of the cut is gelatinous, with an abundant separation of the aqueous exudate. In the course of the vessels, hemorrhages are noted.

Examples: inflammation of the skin in the first degree of burn, changes in the surrounding tissue of submandibular, occipital lymph nodes in anthrax in pigs.

During the chronic course hyperimia fades, hemorrhage is less manifested, CT grows.

2.Serous-inflammatory hydropsy: accumulation of serous exudate in the natural closed cavities of the body (pleural, abdominal, etc.). Serous membrane when it is turgid, dull and congested with hemorrhages.

Examples: serous peritonitis, pleurisy, arthritis, etc.

3.Bullous inflammation: this is the accumulation of serous exudate under the epidermis with the formation of a blister (bull).

Etiology: minor burns, frostbite, effects of weak inflammatory agents, calluses, viral infections (herpes, foot and mouth disease).

Clinical significance: mild inflammation with a favorable outcome. The exudate dissolves well. Excessive accumulation of exudate can lead to hypoxia and organ failure.

56

Fibrinous inflammation

It is an inflammatory reaction with the formation of a dense exudate rich in fibrinogen, turning into the affected tissue into insoluble fibrin. This is facilitated by the release of tissue thromboplastin. In addition to the fibrin part of a fibrinous exudate polymorphonuclear leukocytes and necrotic tissues are composed. Fibrinous inflammation is more often localized on the serous and mucous membranes.

Etiology: bacteria, viruses, exo - and endogenous chemicals. Morphology: fibrinous inflammation occurs with a gradual

accumulation of fibrin. In the beginning it is elastic, translucent grayyellow mass. Then they lose their transparency, become dry, over time, compress into easily friable mass of gray-white color. Depending on the localization of fibrin, fibrin inflammation is divided into:

1.Croupous (surface): fibrin deposition on the surface of natural cavities and mucous membranes. This is preceded by a powerful hyperemia and the transformation of fibrinogen into fibrin. Signs of major inflammation: a fibrin pellicle is formed on the serous, mucous membranes of the articular covers, which is easily removed, exposing the swollen, hyperemic dull shell of the organ. Over time, the pellicle thickens, compacts, becomes similar to the felt and can be rejected, forming a mold of the cavity where it was formed, or fibrin masses germinate CT and fit tightly to the body. For example, "hairy heart" in pericarditis. In this case, the pericardium fuses with the epicardium. Synechiae develop (adhesions). The accumulation of fibrin in the alveoli in case of major pneumonia – in the lumen of the alveoli at the beginning white blood cells and plasma protein accumulate, and then the protein is converted into insoluble fibrin, sealing the alveoli.

2.Diphtheritic (deep) fibrin inflammation develops when fibrin is deposited between the cell elements in the depth of the tissue, so the tissues undergo atrophy, dissolve, and fibrin penetrates deep into the necrotic tissue. Such inflammation is characterized by the fact that the fibrin pellicle is tightly connected to the wall of the organ and, if rejected, then a long-lasting defect, erosion or ulcer is formed. As a rule, on the border between the diphtheria inflamed focus and a relatively healthy tissue, there is a demarcation inflammation in the form of a red border, in which hyperemia of the vessels and intense cell infiltration are detected. For example, diphtheritic colitis in classical swine fever.

57

Clinical significance: a mixed record. On the mucous membranes erosion and ulcers may form. In the lung in croupous pneumonia the exudation is melted, but when insufficient expansion occurs outgrowth CT with carnification of lungs, when excessive activity of neutrophils can be observed the development of an abscess, gangrene, fistula. On serous membranes fibrinous exudate can melt (but most often adhesions form, that is, growing CT).

3. Purulent inflammation – characterized by the formation of exudate with a predominance of altered leukocytes. Purulent exudate is built on the principle of: purulent taurus + purulent serum. Purulent corpuscles are leukocytes (primarily neutrophils) in the state of dystrophy and necrosis, which break down and release enzymes. Purulent serum is a liquid that is formed under the action of the above enzymes. Pus is rich in proteins and shaped elements. It is divided into benign (there are more purulent cells than purulent serum) and malignant (there is more purulent serum). Benign pus develops with increased resistance of the body, malignant – with reduced. The etiology of purulent inflammation: purulent inflammation is caused by pyogenic bacteria (staphylococci, streptococci, diplococci, mycobacteria, brucella, pathogenic fungi, some chemical agents such as turpentine, kerosene, toxic substances).

Specific features of inflammation in farm animals

Species of animal has a significant importance in the occurrence, development and outcome of the inflammation caused by the same phlogogen. Due to the evolutionarily developed metabolic processes, the peculiarity of morphology and physiological constants, specific and non-specific factors of protection, the reaction to damage of different origin in animals is different. In aseptic inflammations caused by physical or chemical agents, the reaction of ungulates and artiodactyls is ambiguous.

In horses, in response to mechanical damage without compromising the integrity of the covering tissues, the development of serous and serous fibrinous inflammation prevails. In cattle, pigs serous-fibrinous and more fibrinous inflammation develop. Exudate is thicker, viscous, yellowish, sometimes with a mixture of red blood cells. Local clinical signs (fever, pain, swelling fluctuation) are less pronounced than in horses.

58

In cloven-hoofed the duration is longer than in ungulates. In experimental playback of inflammation chemical phlogogen (calcium chloride, croton oil, turpentine, chloral hydrate), introduced parenterally in horses purulent-necrotic inflammation with formation of cavity, filled with pus develops. In the subsequent abscess spontaneously opens. Recovery occurs after complete rejection of necrotic tissues, stopping the separation of purulent exudate from the cavity.

In cattle, sheep, pigs in response to parenteral administration of similar chemicals there is a response in the form of fibrinous-necrotic inflammation. It can be completed by resorption and neutralization of the chemical, encapsulation of the stimulus, sequestration with the formation of purulent exudate.

The introduction of turpentine subcutaneously in the region of the horses dewlap is always accompanied by the development of purulent inflammation on the injection of the stimulus. The abscess is formed and spontaneously opens after 90-120 hours after the injection of the stimulus. Flowing pus is white, of creamy consistency. Injection of turpentine into the breastplate ends in cattle resorption of inflammatory edema for 1.5-2 months, and in sheep and pigs — for 10-15 days. Abscessing in cloven-hoofed animals, in contrast to horses is not observed.

Inflammation caused by the ingress of microorganisms into the tissues also occurs ambiguously in different animals.

Septic inflammation occurs in traumatic injuries, when the integrity of the covering tissues is violated, when the gates of infection are open, and with specific infectious diseases (tuberculosis, brucellosis, glanders, salmonellosis, etc.).

Purulent form of inflammation is induced by streptococci, staphylococci, E. coli, Brucella, Salmonella, other pathogens.

Putrid inflammation occurs when anaerobic microorganisms enter the tissues. The reaction of different animals to infection with microbes of the same virulence is ambiguous.

Thus, in dogs and cats, a typical staphylococcal infection prevails

— Staphylococcus pyogenes aureus, in horses — Streptococcus equi. In large and small cattle, pigs purulent inflammation (up to 80-

90% of all purulent forms of inflammation) is caused by the association of coccal forms of microorganisms with E. coli, Proteus, other pathogens.

59

Sheep, unlike other animals, are very sensitive to anaerobic infection from the Clostridium group.

Septic inflammation in animals has a two-phase course. In the first phase, there is neutralization and removal of the stimulus from the body, in the second phase there is a restoration of the defect of the damaged tissue.

In horses, the first phase is manifested by three clinical and morphological stages:

1.the formation of swelling due to serous or sero-fibrinous exudate;

2.the formation of a cavity filled with purulent exudate;

3.necrosis of tissues, removal of purulent masses by spontaneous opening of the abscess.

Loss by exudation of a large number of irreplaceable protein leads wounded horses to exhaustion, cachexia.

In cattle, sheep, pigs not three, but four stages of development of septic inflammation are observed:

1.edema due to fibrinous infiltration, fixation of microbes at the site of introduction of pathogens into the body;

2.organization of fibrin, encapsulation of the stimulus by connective tissue. At this stage, the process can be completed, as the neutralization of the microbial stimulus happens. If it continues its action, the inflammation goes into the third stage;

3.formation of a capsule-limited cavity. At this stage, the process can be completed by germination of the abscess with connective tissue;

4.spontaneous opening and removal of the stimulus from the body. In cattle, the main stage of septic inflammation is the second, during

which the stimulus is encapsulated.

60