Inflammatory process in veterinary medicine: development mechanisms and classification

Inflammation is a complex response of the organism to the influence of various pathogenic irritants, manifested (at the site of their impact) by a complex of functional and structural changes in the form of tissue metabolism disorders (dystrophy), blood circulation disturbance (exudation), and cell proliferation.

Inflammation is a protective reaction of the organism; it is the most common pathological process that underlies many diseases, for example, pneumonia, gastritis, etc.

Exogenous: mechanical, physical, chemical, and biological agents.

Endogenous: circulatory tissue disorders, the impact of pathological metabolic products, and neurotrophic disturbances. The intensity of the inflammatory process is determined by the properties of the pathogenic agent, the location of the process occurrence, tissue characteristics, and the state of the organism.

Redness is associated with an influx of arterial blood; subsequently, the inflamed area turns blue, which is associated with blood stasis. Swelling of the inflamed area is linked to blood influx and the leakage of exudate and leukocytes, as well as abundant proliferation. Temperature increase is associated with increased metabolism and arterial blood influx. Pain arises from the mechanical pressure of the exudate on nerve endings and their irritation by toxic products. Function disorder is a consequence of impaired nutrition, innervation, and metabolism in the inflamed area.

Any inflammation is characterized by three main, interrelated phenomena:

2) exudation and emigration (circulatory disorder),

In various inflammations, different of the listed moments may predominate: if the process of tissue destruction is distinctly expressed, inflammation is called alterative; with a predominance of vascular reaction, it is exudative; with a prevalence of tissue growth, it is proliferative.

Alteration (from Lat. change) is characterized by damage, dystrophy, necrosis (dying off), and rejection of cellular structures. If these changes are observed from the direct action of an inflammatory agent (burn, injury, electric shock), then the alteration is called primary. If, however, changes of this kind develop in the course of the inflammatory process, it is secondary alteration. Dystrophy is a violation of nutrition and metabolism, manifesting in the degeneration of cellular elements, swelling, and dissolution of intercellular space fibers. With severe damage (burns), necrotic processes predominate. In the center of the inflammatory focus, a decrease in metabolism is observed, whereas around metabolism is increased — "metabolic fire."

The vascular reaction during inflammation is characterized by vessel dilation and an influx of a large amount of blood — arterial hyperemia. The vasodilating effect is caused by the influence of under-oxidized metabolic products: albumoses, peptones, histamine, and acetylcholine. However, veins do not dilate but even constrict; blood stasis is observed, and hyperemia becomes venous. In the slowed blood, a redistribution of blood elements occurs: leukocytes move to the vessel wall and adhere to it — marginal leukocyte positioning.

Exudation and tissue defense mechanisms

Exudation — the oozing of fluid during inflammation from vessels into tissue. Inflammatory effusion accumulating in any cavities (thoracic, abdominal) is called exudate, and that which permeates any tissue is called infiltrate (Lat. to permeate).

Exudate, unlike transudate, contains more protein (more than 3%), is characterized by the presence of leukocytes and even erythrocytes, as well as pronounced proteolytic properties. Exudation has a protective-physiological significance:

• Exudate dilutes and thereby reduces the damaging effect of the inflammatory agent.
• Exudate, due to the presence of enzymes in it, neutralizes toxic substances.
• Exudate possesses bactericidal action.

Leukocyte emigration and proliferative processes

Leukocyte emigration — the exit of leukocytes through the vessel wall into the tissue. It occurs simultaneously with exudation. I.I. Mechnikov explained leukocyte emigration by chemotaxis — a peculiar, attracting action of chemical substances formed in the inflammatory focus on leukocytes.

Emigration is preceded by marginal leukocyte positioning, especially in venous capillaries. After this, leukocytes begin to penetrate through the dilated pores of the vessel wall already an hour after the impact of the inflammatory irritant. Initially, leukocytes form peculiar protrusions, pseudopodia, which penetrate into the pores of the vessel endothelium. Then the body of the leukocyte completely flows out of the vascular bed (phenomenon of leukocyte emigration).

After this, they move with amoeboid movements toward the center of the inflammatory focus, where they perform a phagocytic function. During this, some of the leukocytes die with the release of enzymes that digest decay products. The remaining part of the leukocytes either emigrates back into the bloodstream or takes part in proliferative phenomena. In purulent inflammations, leukocytes accumulate in huge quantities (pus is mainly dead leukocytes).

Figure 6 – Inflammation of the frog mesentery: a – leukocytes that have exited into the tissue; b, g – leukocytes migrating from the vessel; v – phenomenon of "marginal leukocyte positioning"; d – eryth-

Proliferation (Lat. to create offspring) — local multiplication of cells and non-cellular elements. It is especially well expressed in the late periods of inflammation and in chronic forms of its course. Proliferative processes proceed particularly actively after the rejection of necrotic masses and the destruction of the pathogenic agent. Under conditions of inflammation, damaged tissues and, especially, blood cells, are sources of humoral factors stimulating tissue multiplication.

The more efficiently the wound is cleared of damaged tissues, the more fully the proliferation of tissue elements occurs, restoring the structure and functional integrity of the tissue. Wound cleansing occurs due to phagocytosis of damaged tissues by leukocytes and macrophages. In this process, the enzymes of microorganisms and the tissue's own enzymes also play an important role.

Proliferation is followed by regenerative processes, which conclude the inflammation. Regeneration is not strictly an inflammatory process; it consists of increasing the reproduction of young granulation tissue. It grows from the periphery toward the center of the inflammation and eventually fills the tissue defect. The growing granulation tissue forms a barrier (demarcation line) between the inflammatory focus and healthy tissue, which prevents the spread of the inflammatory focus to surrounding tissues.

Alterative inflammation is characterized by a predominance of dystrophy and necrosis in tissues, with weakly expressed exudation and proliferation. Such inflammation is pronounced in the brain, heart, and liver.

Exudative inflammation is characterized by a marked vascular reaction: 1. Serous inflammation - the exudate is a clear liquid containing 5-6% protein and a small number of formed elements; it occurs in cases with a favorable course of inflammation. 2. Serous-catarrhal inflammation - develops on mucous membranes; serous exudate reaches the surface along with mucus, with few leukocytes. 3. Fibrinous inflammation - with the exudate, a large amount of plasma proteins is released, including large protein molecules of fibrinogen; the latter coagulates outside the vessel wall, forming on the surface a film, consisting of a fibrin network infiltrated with leukocytes. 4. Hemorrhagic inflammation - when erythrocytes are mixed into the exudate. 5. Purulent inflammation - accompanied by the release of purulent exudate, a thick yellow liquid with a high content of leukocytes and various tissue elements at different stages of destruction. Types: a) empyema - an accumulation of pus in any closed body cavity (empyema of the pleural cavity, abdominal cavity, gallbladder, etc.). b) abscess - an accumulation of pus in an artificial cavity formed due to tissue necrosis and liquefaction at the focus of inflammation. c) furuncle - purulent inflammation of sebaceous glands and hair bulbs. d) carbuncle - purulent inflammation of a group of sebaceous glands and hair bulbs. e) fistula - an encapsulated passage connecting a deep-seated focus of purulent inflammation with the external environment. Through the fistulous tract, pus flows outward. f) phlegmon - diffuse purulent inflammation spreading through loose connective tissue. g) pyemia - general infection of the organism with the formation of multiple

Putrid inflammation develops when putrid microflora enters the focus of inflammation. It can be gangrenous, tending to spread gradually, and ichorous - with an unpleas-

Proliferative inflammation - the growth of new tissue elements predominates over all other tissue elements - in cases of glanders, actinomycosis, and tuberculosis.