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The body defense attempt to dest roy any irritant cross the epithelial barrier by the help of inflammatory barrier. Inflammation derived from the Latin inflammare meaning to set afire. The response of a higher animals exposed to an irritant is called inflammation. Inflammation is a protective response of the body to eliminate the initial cause of cell injury resulted from the irritant. Also inflammation is defined as complex progression vascular and tissue changes of the living tissue develop in response to an irritant, which is not severe enough to cause necrosis. Moreover the definition proposed by Ebert is more complete: inflammation is a process which begin following sub lethal injury to tissue and end with complete healing.
The inflammatory process is designed to inactivate and remove the injuries agent, remove any damaged tissue resulting from the injury, and help repair and healing. The inflammation carries the suffix “itis” which is quite specific, for example endocarditis and enteritis, Exceptions as pneumonia and pleurisy, which equal pneumonitis and pleuritis respectively.
Inflammation is caused by living and non-living agents that have the capacity to injure living tissue. 1. Pathogenic organisms including bacteria, viruses, fungi, protozoa and parasitic. 2. Chemical poisons. 3. Mechanical and thermal injuries such as burns, excessive cold and trauma. 4. Immune reactions includes hypersensitivity and autoimmune diseases.
The inflammatory process is composed of many interacting parts, which seem to be unrelated to one another but each functioning to create the morphologic signs associated with this reaction. There are four major components of inflammation: 1. Plasma protein, which lack through the blood vessel wall causing swelling. It contain albumin, immunoglobulins and other proteins as zymogene, which activated and causing the initiation of complement, fibrinolytic, coagulation and kinine system. 2. Fixed tissue cells such as mast cells, fibroblasts and endothelium are very important for initiation and maintaining the inflammatory process through secretion of chemical mediators 3. Leukocytes which arrive to the inflamed area are important to phagocytize and degrade the organisms and debris while platelets do its function through secretion of chemical mediators 4. Mediators of inflammatory reactions consist of protein lipids and vasoactive amines secreted by the above mentioned and play an important role in inflammation.
Clinically, acute inflammation is characterized by 5 cardinal signs: redness (Rubor), hotness (Calor), swelling (Tumor), pain (Dolar) and loss of functions (Functio laesa). Redness and hotness results from the increased flow of blood carrying warmth from the higher interior temperature of the body to the periphery. Swelling is due to accumulation of fluid. Pain is due to release of chemicals that stimulate nerve ending. The loss of function is due to a combination of factors.
It includes vascular and exudative changes (Fig. 1). The inflammatory process, especially acute inflammation, is primarily circulatory phenomenon involving the blood vessels and flow.
Changes in blood flow in inflammation I) Changes in caliber and vascular flow: a) Transient constriction of the arterioles immediately after injury results from smooth muscle contraction of the arterioles, which mediated by damaging stimulus. It disappears within 3 to 5 seconds. b) Long-standing vasodilatation which first involves the arterioles and then venules and resulted in opening of new microvascular beds in inflamed area, with increased blood flow and cause the tissue become hyperemic, red and warm. Chemical mediators, mainly prostaglandin, are responsible for dilatation of arterioles. It lasts throughout the stage of acute inflammation to bring extra blood to the inflammatory area. C) Slowing and stasis of blood flows due to increase permeability of the microvasculature resulted in outpouring of protein rich fluid (exudate) into tissue leading to increase viscosity. Moreover, Impaired gliding action of plasmatic zone which exchanged position with the axial (cellular) stream besides adhesion of leukocytes and the swollen endothelial cells inside the Lumina of blood vessels resist blood flow
The permeability of capillaries and venules is the function of inter cellular junction between the endothelium. Small molecules normally pass through pores but pinocytosis permits passage of large one. Increased vascular permeability is one of the clearest changes that occur during inflammation leading to swelling or edema. The edema occurs due to increase the collection of fluid than removal by lymphatic. Active contraction of endothelial actin filaments or direct damage of endothelial cells produces increased permeability.
1. Immediate transient response occurs due to mild injury and lasts for 30 minute under the effect of chemical mediators. This response occurs mainly in post capillary venules 2. Immediate sustaineal response occurs immediately after severe injuries and lasts for several hours to several days. It involves all vessels leading to increase vascular permeability and the formation of inflammatory exudate. 3.Delayed prolonged response occur due to mild to moderate injury starting after injury peaking 2 to 6 hours and gradually subsides by 8 hours as in case of sunbathing.
The passage of large amount of fluid from the circulation to the interstitial tissue produces swelling. The composition of exudate approaches that of plasma. The exudate dilutes the irritant. Moreover, the fibrin acts as physical barrier to prevent spreading of irritant besides it contain antibodies used to distract the irritant. The exudate brings phagocytic cells that distract and remove the irritant and necrotic tissue and help healing (Fig 2). Lastly plasma bring all the component of plasma enzyme systems (coagulation cascade, fibrinolytic system and complement cascade) which share in initiation, control, and resolution of inflammatory process. These enzyme systems are a complex interrelating process that produces biologically active molecules and peptide fragments.
The movement of leukocytes from blood to the area of inflammation is one of the most important manifestations of acute inflammation. The inflammatory cells (granular and a granular) are responsible for killing bacteria, secrete cytokines, enzyme and oxidizing reagent to regulate inflammatory process and removal of necrotic tissue to help healing process. The migration of cells occurs primarily from venules soon after the vascular changes occur where neutrophils are usually first to leave and gain exit
The sequence of events in the extravasation of leukocytes from the
vascular lumen to the extravascular space can be divided into 4
steps (Figs 3 & 4)
Erythrocytes enter the inflamed area passively under the effect of hydrostatic pressure (diapedesis)
1. Recognition and attachment of leukocytes to most microorganisms is facilitated by serum protein called opsonin. 2. Engulfement: The foreign particle is engulfed by phagocytic cells forming phagocytic vacuole. The phagocytic vacuole fuse with lysosome to become a phagolysosome in which the ingested particle is exposed to the lysosomal enzymes. Some of the enzyme kills microorganisms, and others digest the remnants. 3. Microbial killing and degranulation by phagosome enzymes (hydrogen peroxidase, myeloperoxidase, toxic oxygen based radicals as superoxide) through oxygen dependent or independent mechanism.
Figure
3: Diagram showing sequence of movement of
leukocytes in inflammatory process (margination, adhesion and
emigration).
Figure
4: Illustration
showing sequence of cellular response in acute inflammation
including margination, adhesion, emigration and phagocytosis.
Figure
5: Diagrammatic
illustration to show the steps of cellular movement and
phagocytosis.
Figure
6: Phagocytosis
represented by engulfing of irritant by macrophages. H&E
Before we go into description of chemical mediators it will be helpful to understand the Triple response of Lewis. The vascular changes resulting from a mild mechanical injury of skin are often referred to triple response of Lewis. This phenomenon is produced by firmly stroking the forearm with a blunt instrument. 1. Within one minute a red line appear along the line of strike as a result of dilatation of arterioles due to smooth muscle relaxation generated by histamine. 2. Soon a red flare spread out from the injured area, as results of vasodilatation of tissue surrounding the injury, (local axon reflex). 3. Wheal forms due to increase vascular permeability leading to exudation of fluid. The red line and wheal mediated by chemical mediators. Mediators are substances that direct the vascular and cellular event in inflammation. They can originate from plasma, cells or damaged tissue. They can be divided into:
Histamine is widely distributed in tissue particularly in mast cells and release in response to variety of stimuli. They cause vasodilatation and increase permeability Serotonin. Like histamine, serotonin is vasoactive amine which play the same role as histamine. It is found primary in platelets. 2. Plasma protease They are three interrelated plasma derived factors
Bradykinin is the final product causing increase permeability and stimulates pain receptors. Kinin are activated by plasma enzymes called kallikrein
Increased hydrostatic pressure and increased vascular permeability in post capillary venules lead to escape of serum into the extravascular space resulted in edema and swelling. The fluid has benefit effect as to dilute the toxic substances, and antibodies against infective agents and lastly plasma enzyme system that initiate, maintain and control the inflammatory process. Coagulation cascade, which either initiated either by activation of extrinsic or intrinsic system, lead to formation of fibrin. The fibrin is very important in inflammatory process because it produces a matrix for chemotactic migration of leukocytes in inflammatory area and provides a barrier to motile organisms. The kinine system participitate in the interinsing coagulation and generation of the vasoactive peptide Bradykinin. The fibrinolytic system is very important in dissolution of the fibrin clot. The complement system either classic or alternate pathway resulted in destruction of cell membrane or production of anaphylatoxins which lead to degranulation of mast cells with release of histamine which cause increase vascular permeability. Moreover, C3b act as opsonin promoting phagocytosis.
The inflammatory cells include granulocytes and agranulocytes.
This group of cells includes neutrophils, eosinophils and basophils
Neutrophils are aggressively phagocytic cells that constitute the
first line of defense against microorganisms. The cells sometimes
known as heterophils, polymorph nuclear, pus cell or granulocytes They occur in pus as the predominant cell in suppurative inflammatory exudate in response to infection by pyogenic bacteria. Neutrophil products include cationic protein, acid proteases and neutral proteases. The cationic proteins increase vascular permeability by releasing histamine from mast cells, are chemotactic monocytes and may inhibit movement of neutrophils and eosinophils. Acid proteases act primarily within phagosomes. Neutral proteases degrade extracellular components such as collagen, basement membrane, fibrin, elastin and cartilage and are thus responsible for the tissue destruction associated with collections of neutrophils in tissue. They can also induce the release of kinins and initiate chemotactic activity from C3 and C5 fragments. The phagocytic processes in neutrophils and macrophages have many similarities. Neutrophils have a half-life in circulating blood of about 6 hours. They leave the blood to go into tissue and don’t return (end cell) and gost of them are lost through mucosal surfaces.
Eosinophils
are white blood cells
that are responsible for combating infection by
parasitic
helminthes and arthropods.
The Eosinophils make up about 1.5% of the total White Blood cells.
The function of eosinophils includes: 1. Limited phagocytic
capability; 2.cytoxicity to helminthes; 3-augmentation of
inflammatory reaction particularly in hypersensitivity; 4. inhibition
of allergic reaction Their red granules on hematoxylin and eosin
staining distinguish them from neutrophils (Fig. 9)
Mast cells and basophils are members of granulocyte family Basophils are found in very low number in the circulating blood meanwhile the mast cells are present in connective tissue. They are present in perivascular area and in blood in small number. Mast cells and basophils both contain receptors for IgE on their cell surface and rich in vasoactive Basophils are involved in delayed and immediate hypersensitivity. The nucleus is lobulated and the cytoplasm contain basophilic granules contain histamine and heparin. The cell surface antigen with antibodies on the surface membrane resulted in degranulation and release of histamine and heparin. Basophils have a life span of 10-12 days and are made in the marrow.
This is a generic term for blood monocytes and the cells to which they give rise. They are important in acute inflammation, as well as being a key element in chronic inflammation. The mononuclear cells includes monocytes (macrophage in tissue), lymphocytes, plasma cells, and giant cells.
Lymphocytes originated from lymphoid stem cell in fetal life and
produced in lymph nodes, bone marrow, thymus and in the lymph
follicles of many mucous membranes (Figs 10 &11)
Lymphocytes can classified into two main classes. The first is called B-lymphocytes and the second is called T-lymphocytes.
T lymphocytes are a group of cells that have passed through the thymus (and been acted on by the hormone thymosin) during early biological life. T-cells are the center-piece of the immune system. T-cells of various sorts are predominant throughout the lymph nodes except in and around germinal centers ( paracortex of lymph nodes), periarterial lymphoid sheath in spleen white pulp. Around 80% of circulating lymphocytes are T-cells. Young T-cells differentiate into many subtypes, which act as regulators and effector. T cells divided according to surface expression accessory molecules into two subsets, T4 and T8. Following activation of T cell by specific antigen, the lymphocytes transform into effector cells T cell. The effector cell can classify to those doing its function after contact with cells or that release of soluble cytokine mediators. Function of effector cells 1. Helper or inducer CD4 T lymphocyte differentiate into cells that produce mediators (lymphokin) that augment the function of other cells. CD4 helper cells secret cytokines that transform B lymphocytes to plasma cells. T-helper cells (TH1) are produce IL-2 and INF-gamma and act on macrophages. TH2 is produce IL-4 and IL-5 and work on the eosinophils. 2. T cell suppressor is a TCD8 cell that suppresses other cells. 3. Cytotoxic lymphocytes have surface antigen and subject to direct cell killing by causing lyses through producing holes in surface membrane of antigen positive cells.
They are a group of T cells (5-10%) of peripheral blood lymphocytes) which do not express T cell receptors on their surface. Some cells are cytotoxic and called natural killer. Natural killer lymphocytes (NK-cells) are bigger than other lymphocytes, and have cytoplasmic granules. They attack and cause apoptosis in cells with altered class I MCH antigens, without being "specially sensitized". The granules, which are injected into the target cell, contain perforin and granzyme, along with other stuff
Another class of lymphocytes, which when activated produce freely circulating immunoglobulins (antibodies). B lymphocytes are responsible for humeral immunity. B-cells predominate in the follicles (germinal centers) of the lymph nodes and are more common than T-cells in the red pulp of the spleen and in the bone marrow. Around 15% of circulating lymphocytes in the peripheral blood are B-cells. Stimulation of B-lymphocytes by specific antigen resulting in formation of plasma cell and synthesize antibodies specific for stimulating antigen. In the germinal centers, antigen-antibody complexes are presented to B-cells by the dendritic follicular cells. B-cells have surface immunoglobulin, Fc receptors, C3b receptors, and CD40.
Plasma cells
form by a process of maturation of conversion from
B-lymphocytes. Their function is to make and store antibody.
Usually, the lymphocyte is directed to made the antibody and during
the process of production becomes a plasma cell (Fig. 12)
Plasma cells are usually present along with lymphocytes in tissue. They are numerous along the sinusoidal lining of and medullae of lymph nodes and the red pulp of the spleen after antigenic stimulation. Plasma cells are rarely seen in circulating blood. The formation of mature plasma cells from lymphocytes requires 4-5 days.
Macrophages (tissue monocytes) are derived from bone marrow. There
are fully differentiated end stage cells that do not, under normal
condition, divide (Fig. 13)
Macrophages modulate the activities of other cells by secreting soluble factors such as interleukin 1 and TNF-alpha as well as some complement components. In addition, macrophages are effector cells when summoned by T-cells or activated complement. They have receptors for the Fc portion of IgG and for various complement components. Activated macrophages can secret neutral protease, killing tumor cells besides killing and control intracellular organisms. Moreover, activated macrophage can secret interferon, endogenous pyrogen and plasminogen. The activated macrophage can synthesize thromboplastin, and prostaglandin besides stimulating fibroblast proliferation and collagen synthesis.
Epithelioid cells are activated macrophages with abundant pale foamy cytoplasm, vesicular nuclei. The epithelioid cells contain numerous mitochondria, Golgi apparatus and abundant rough endoplasmic reticulum. They are less phagocytic than macrophages. The ultra-structure suggested that the function is mainly secretory rather than phagocytic.. Epithelioid surface properties seem to be changed so that they lie closer to each other similar to prickle cells in the squamous epithelium.
The giant cells are formed by fusion of the cytoplasm of macrophages.
There may have two to three or up to two hundred nuclei. There have
3 types of giant cells can seen in tissue. Langhan’s cells with
nuclei around the periphery (Fig. 14)
Figure 7:
Microscopic picture of neutrophils in suppurative
meningioencephalitis showing polymorph nucleus. H&E
Figure 8:
Mammalian blood film showing neutrophils characterized by segmented
nucleus.
Figure
9: Liver showing eosinophils
aggregation. The eosinophils characterized by segmented nucleus with
eosinophilic cytoplasmic granules. H&E
Figure
10: Acute
lymphocytic inflammation showing aggregation of lymphocytes
characterized by dark non segmented nucleus. H&E
Figure 11: Blood
film showing lymphocytes
characterized by dark non segmented nucleus.
Figure 12: Electron
micrograph of pasma cells.
Figure 13: Lymph
node of cattle suffering from chronic lymphadenitis showing aggregation
of macrophages. H&E
Figure 14:
Granuloma showing
Langhan's
giant cell characterized by nuclei placed around the periphery
(horseshoe). H&E
Inflammation can be classified based on the following characters
1. Adequate inflammation. It occurs when the body reaction is sufficient to overcome the irritant and leading to complete healing.
We can classify inflammation according to the length of inflammatory process into:
2. Acute
inflammation
usually takes a short time to appear and disappear. The inflammatory
cells mainly neutrophils in bacterial infection and eosinophils in
helminthes infestation (Fig. 16)
3. Chronic
inflammation:
it take long time due to the irritant has low intensity that dose
not able to stimulate the body defense to overcome it. It is a
proliferative and appear highly cellular. The main leukocytes are
macrophages, giant cells and plasma cells (Fig. 17)
The inflammation can classify into hyperplasic, hypertrophic, fibrous or atrophic.
inflammation.
Acute
inflammation is of relatively short duration and characterizes by
fluid exudation and predominantly neutrophilic leukocyte
accumulation.
The acute inflammation has two major
components, vascular changes and cellular event (Fig. 18)
The inflammatory process is composed of many interacting parts, which seem to be unrelated to one another but each functioning to create the morphologic signs associated with this reaction. There are four major components of inflammation
Acute inflammation can be divided according to the predominant type of exudate into.
Definition: It is a mild inflammation characterized by the exudation of blood serum. Serous exudate is composed primarily from clear fluid and its presence indicates mild irritant. This is the form which equivalent inflammatory edema.
This type of inflammation usually caused by a variety of mild irritants, many of which are transient. Many mild irritants as sun rays, viral infection, trauma besides inhalation of gasses and chemicals can induced serous inflammation.
vascularized surface. Moreover, we can see serous inflammation in skin associated with some viral diseases and burn. In lungs we see serous inflammation in early stage of pneumonia.
The large amount of albumin in tissue appears as homogenous
eosinophilic granular material. The cells in tissue are spread apart
by serous fluid serving to dilute the irritant. Few leukocytes
mainly neutrophils are usually seen beside congested and dilated
blood vessels (Fig. 19)
Figure
16: Microscopic picture of brain showing
acute inflammation. The inflamed tissue shows congested and dilated
blood vessels and inflammatory cells mainly neutrophils. H&E.
Figure
17:
Microscopic picture of chronic inflammation. The inflammatory cells consisted mainly
from macrophages and giant cells.
Figure
18: Lung showing acute suppurative
inflammation characterized by vascular (congested blood vessel) and cellular reaction
(Neutrophils). H&E
Figure
19: Lung,
Micro, serous inflammation. The alveoli contain pale eosinophilic
fluid and inflammatory cells. The interalveolar capillaries are
congested. H&E.
A watery fluid is seen accumulate in the body cavity, in tissue space or flows from the cut surface of tissue or organ. The cardinal signs of inflammation are present. Cloudiness of serous membrane is noticed due to presence of some inflammatory cells
The presence of serous exudate is useful to dilute the irritant and weakening its local effect. Moreover, the swelling of the affected tissue interferes of its function. It indicates that the cause is mild, and prognosis is usually good. The fluid is resorbed if the cause is overcome.
Definition: It is characterized by main component of inflammatory exudate is mucus. It is mild inflammation occurs on mucous membranes. Mucus is produced by hyperplastic goblet cells with liberation of large amount of mucus. The mucus protect the underline mucous membrane and when expectorated remove much of debri and irritants. Moreover, it contains many antimicrobial substances.
The irritants which cause this type are mild and of short duration as chemical (formaldehyde and cresol when inhaled or used in a great concentration), inhaled dust, cold air or foreign protein. Moreover, infections as in some viral and bacterial diseases besides ingestion of spoiled or irritating food.
The mucus is stained pale bluish or grayish by H&E and red by
Thionine or mucicarmine. Hyperplasia of the goblet cells may be
conspicuous. Affected epithelium appears hyperplastic and many of it
may be desquamated as in the lumen of bronchioles. The affected
mucous membrane show congested blood vessels and infiltrates with
inflammatory cells (Figs 20, 21,22 & 23)
The presence of clear, slimy mucus is the characteristic signs of
catarrhal inflammation (Fig. 24)
The mucus tends to protect and was the mucous membrane. If the cause is removed the flow of mucus subsides and the damaged epithelium is regenerated but if it persists for a long period; another type of severe inflammation may develop.
Definition: It is a severe inflammation characterized by an exudate containing large amount of fibrin. The presence of fibrin indicates a severe acute vascular injury. It usually involves serous and mucous membranes. Injury of the endothelium and the basement membrane allow leakage of fibrinogen, which polymerize perivascular as fibrin. Grossly fibrin exudate appears as tan stringy, shaggy meshwork on tissue surface. Fibrin creates a network in tissue space that prevent spread of irritants. Moreover, clotting in lymph vessels prevent migration of bacteria laden leukocytes. Fibrinous exudate may be so severe that damage the tissue.
Fibrinous inflammation usually results from severe irritants that lead to damage the wall of blood vessels and permits the escape of fibrinogen, which is the largest molecules of plasma proteins which polymerize perivascular as fibrin. It is associated with some bacterial diseases. Prominent among these are Diphtheria bacillus, Clostridium and Shigella species. Moreover some viral diseases (as infectious laryngotracheitis and feline enteritis), and inhalation of hot gases during bran fires produced fibrinous inflammation.
Figure
20: Intestine showing catarrhal inflammation. The epithelial lining of
intestinal villi changed to goblet cells. The lamina propria
infiltrated with inflammatory cells besides congested blood vessels.
H&E.
Figure
22: Bronchi
showing catarrhal bronchitis characterized by increase number of
goblet cells beside infiltration of the lamina propria with
inflammatory cells. H&E.
Figure
24: Sheep
showing bilateral catarrhal nasal discharge.
Figure
25: Trachea,
Micro, Fibrinous inflammation. The trachea of chicken infected with
ILT showing complete desquamation of epithelial lining and the
fibrin and necrotic materials covered congested lamina propria. H&E.
Fibrin, which stained dirty very eosinophilic pink, finely beaded
strands or solid clumps with H&E, is seen attached to the inflamed
surface. The vascular and exudative alterations of inflammation are
present (Figs 25, 26 & 27)
Hyperemia and hemorrhage may be apparent with fibrinous exudate. An
early lesion on a serosal surface gives a roughened ground glass
appearance. Bread and butter appearance is seen when fibrin present
in large quantity. The
affected mucous membranes and the normal
glistening serous membranes appear dull with whitish shreds or
fibrin hanging from them (Fig. 28)
The fibrin serves a number of useful purposes. It may prevent blood loss from the damage surface. Fibrin helps to prevent the spreading of infection by occlusion of the blood vessels and lymphatic in the affected area. It helps phagocytosis and chemotaxis of inflammatory cells. Fibrinous inflammation indicates a severe cause and a bad prognosis. If the inflammation terminates with reasonable promptness, the underlying surface is regenerated and fibrin is dissolved. If the fibrin remain for some days the exudate may be organized and leaves a permanent damage and adhesion.
Definition:
It is a type of inflammation characterized by the formation of large
quantities of pus or the predominant constituent of exudate is
neutrophil. Suppuration is the process of pus formation. and
requires necrosis, neutrophils and proteolytic enzymes. The term
suppurative inflammation indicate a pus run from the surface or fill
cavities (Figs 30, 31 & 32)
Purulent or suppurative inflammation is caused by pyogenic bacteria, as Staphylococcus, Streptococcus and Corynebacterium. Some chemicals as the oil of turpentine, if injected in tissue cause suppurative inflammation. The Presence of considerable numbers of neutrophils in or on a tissue is sufficient for diagnosis. Numerous neutrophils, living and dead are the predominant constituent together with necrotic debris. Vascular and exudative alterations of inflammation are present. Generally, the main constituents of pus are: dead (pus cell) and living neutrophils necrotic tissue and causative agent may or not be seen.
Figure
26: Trachea of chicken infected with ILT
showing fibrinous inflammation. The fibrin threads form mass inside
the tracheal lumen. H&E
Figure
27: Lung,
Micro, fibrinous inflammation.
The alveoli are filed with fibrin threads beside inflammatory cells
and congested interalveolar capillaries. H&E.
Figure
30: Lung showing suppurative inflammation.
The pulmonary tissue is focally replaced by neutrophils beside
congested blood vessels. H&E
The exudate is mainly pus, which is varying greatly in color from
white, yellow, green, red, and black to blue according to the
species of animal and type of bacteria. Streptococcus and
Staphylococcus usually produce white or yellow pus. Corynebacterium,
particularly in bovine produces greenish pus (Figs 30 & 31)
Pseudomonas aeroginosa produces bluish-green pus. Localize suppurative inflammation is called abscess. An abscess is defined as localized collection of pus. The abscess is surrounding by a wall of fibrous tissue. It may be vary from microscopic to large one. A pustule is an abscess in the malpighian layer of the epidermis. Fruncle is a small abscess in hair follicle, while carbuncle is a subcutaneous abscess with several opening. Empyema is the accumulation of pus in body cavities. Pyorrhea is a deep suppurative inflammation of the gum, while phlegmon or cellulitis is a diffuse suppurative inflammation in loose connective tissue, mostly subcutaneous. The consistency of pus varies in different species due to the variance of the proteolytic enzymes present inside neutrophils in various species. The pus of dog is liquid, but viscid in bovine. Pus of birds is dry, caseous because of the presence of an antitryptic enzyme.
The liquifactive necrosis of tissue as a result of suppurative inflammation indicates that the suppurative inflammation is a violent reaction against irritant. Suppurative inflammation usually indicates the presence of a bacterial infection. The presence of pus indicates that the body defense is functioning; hence it is a healthy sign. Suppurative inflammation may lead to pyemia and death.
Definition: It is a severe inflammation characterized by large number of erythrocytes that leave their normal channels by diapedesis. This usually occurs in organs with an abundant blood supply and much surface area such as lungs and intestines. Causes The injurious agent is highly virulent microorganisms (Viral as infectious laryngotracheitis, bacterial as leptospirosis) and acute poisoning by certain chemicals. Among these substances, phenol, arsenic, chloroform and phosphorus are most important.
The affected tissue shows free extravasated erythrocytes, fibrin and
tissue debris. The vascular and exudative alteration characteristic
for inflammation predominant constituent of exudate, but
neutrophils, lymphocytes, plasma cells and macrophages are frequent
(Figs 33, 34 & 35)
Figure
31: Lung suppurative inflammation. The
pulmonary tissue is focally replaced by neutrophils beside congested
blood vessels. H&E
Figure
33: Brain showing microscopic picture of, hemorrhagic inflammation. The predominant cells are
erythrocytes beside congested blood vessels and leukocytic
infiltrations. H&E.
Figure 34:
Brain,
Micro, hemorrhagic inflammation. High power of the previous figure
to show the inflammatory exudate consists from erythrocytes and
neutrophils.
H&E.
Blood colored material, sometimes fluid or clotted are seen on the
surface or in tissue spaces (Figs. 36 & 37)
It indicates that the cause is severe and the prognosis is poor. Animal may die from anemia and extensive tissue damage. Recovery is usually delayed.
Definition: It is a special type of inflammation characterized by predominance of lymphocytes in the exudate and by the absence of the cardinal signs of inflammation.
Viral infections and intoxication generally cause it. The relatively mild toxins as those of plants, result in lymphocytic aggregations in the portal tracts.
The dilatation of blood vessels isn’t outstanding. The exudate is
highly cellular (lymphocytes). Macrophages may be seen removing the
necrotic debris. In the central nervous system, lymphocytes usually
accumulate in the Virchow Robin spaces causing perivascular cuffing
(Figs 38 & 39)
Lesion is usually not recognized and the cardinal signs of inflammation aren’t seen. Grayish white spots of irregular shape and size may be seen mostly in parenchymatous organs.
It indicates the presence of a viral disease or toxemia. If the irritant is overcome; healing occurs rapidly.
Definition: It is a type of inflammation, where the predominant constituent of exudate is eosinophils in association with serous, fibrinous, suppurative or hemorrhagic inflammations.
Hypersensitivity, metazoon parasites and sodium chloride toxicosis in particular species as pigs.
Numerous eosinophils are present beside the other inflammatory
cells
and the vascular reaction (Figs 40, 41& 42)
Figure 38:
Brain,
Micro, lymphocytic inflammation. The lymphocytes are seen in Virchow
Rubin space. H&E.
Figure 39:
Liver showing lymphocytic inflammation. The portal area infiltrates with
lymphocytes besides congestion of portal blood vessel. H&E
Figure 40:
Lung of mice infested with Schistosoma mansoni
showing eosinophilic inflammation represented by peribronchial
aggregation of eosinophils. H&E.
Depends upon cause.
The acute inflammation is aimed to neutralizing or inactivation of the injury. There are several possible outcomes 1. Resolution. Inflammation is said to resolve when no structural cells have been lost after the inflammatory process is complete and phagocytosis has cleaned up the area. It occurs in uncomplicated cases after removal of the cause. 2. Repair. It occurs when tissue necrosis happened. After neutralizing the causative agents, the necrotic tissue removed and healing occurs. 3. Suppuration. It occurs when invasion by pyogenic microorganisms occur. 4. Chronic inflammation. When the causative agents is not neutralized the acute inflammation mount the immune response, which lead to chronic inflammation.
Definition: Chronic inflammation is the response of tissue against injurious agent that persists for a long time. The tissue affected by chronic inflammation usually show immune response, phagocytosis, necrosis and repair. Chronic inflammatory process is usually productive or proliferative rather than exudative.
Chronic inflammation usually develops following acute inflammation due to persistence of infection. Chronic inflammation usually follows repeated acute inflammation Moreover, It may be primary develop due to a low grade of tissue response to persist infection with intracellular microorganisms as Mycobacterium tuberculosis, prolonged exposure to non degradable but potent toxic substance as silicosis and immune reaction as type IV hypersensitivity. The affected tissue in chronic inflammation usually shows the following characters Immune response represented by plasma cells, lymphocytes and macrophages. Moreover, phagocytosis, necrosis and repair, which characterized by presence of newly, formed capillary and fibrous tissue proliferation and collagen fiber deposition
The characteristic feature of chronic inflammation is infiltration
of tissue with mononuclear cells specially macrophages, lymphocytes
and plasma cells besides newly develop blood vessels, fibroblast
proliferation and collagen fiber deposition (Fig. 43)
Chronic inflammation is characterized by absence of cardinal signs of inflammation. The inflammatory area is indurated and grayish white in color. Moreover the inflammation may be not noticed.
Figure 41:
Liver of mice infested with Schistosoma
mansoni showing eosinophilic inflammation. The hepatic parenchyma is
infiltrated with eosinophils. H&E.
Figure 44:
Peritoneum, Gross, granulomatous inflammation.
Figure 45: Lymph
node, Micro, granulomatous inflammation.
Granulomatous inflammation is a special kind of chronic
inflammation, which occurs in the presence of indigestible material
and/or cell-mediated immunity. Moreover, granulomatous inflammation
is a type of chronic inflammation characterized by presence of
granuloma (Fig. 44)
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Inflammation
