Suppurative inflammation:
Suppuration means liquefaction of necrotic tissue with the formation of pus. It is caused by suppurative or pyogenic organisms such as: staphylococci, streptococci, gonococci, meningococci, and. E-coli
■ These organisms cause necrosis of the tissue with the release of leucotaxin which is chemotactic to neutrophils. Large numbers of neutrophils reach the area of inflammation, some will die producing pus cell which will release proteolytic enzymes leading to liquefaction of the necrotic tissue and fluid pus is thus formed.
■ Some pyogenic organisms produce coagulase enzyme which helps in localization of the inflammation while other organisms produce hyaluronidase enzyme with spreading of the inflammatory process by liquefying the ground substance of the fibrous tissue.
Accordingly we have two types of suppurative inflammation:
a. Localized suppurative inflammation
b. Diffuse suppurative inflammation
A. Localized suppurative inflammation 1. Abscess
Definition: it is an acute localized suppurative inflammation caused by staphylococci mainly which produce coagulaze enzyme. Pathogenesis:
■ The causative organisms (the most common is staphylococcus) are introduced to the tissues, multiplying rapidly, and producing large amounts of bacterial toxins that become concentrated in the center leading to necrosis of tissues.
■ The vascular phenomenon is apparent in the still living peripheral zone which surrounds the central necrotic area. This is sometimes called pyogenic membrane in which there is active hyperemia with many dilated blood vessels and large number of neutrophils. There is also fibrin network leading to localization of infection in this area.
■ Because of the strong chemotactic substances produced, great numbers of leucocytes migrate to the inflammatory area to attack and kill the organisms.
■ Many leucocytes are killed and transformed into pus cells which will release proteolytic enzymes. These enzymes start to liquify the necrotic tissue separating it from the surrounding tissue and are called slough. Later on liquefaction is completed with formation of the fluid pus.
■ The abscess enlarges in size by further necrosis and liquefaction of the pyogenic membrane which will move further outside. The enlargement of the abscess takes place in the direction of the least mechanical resistance.
■ When the necrotic tissue liquify it breaks into small molecules which raise the osmotic pressure in the abscess cavity and thus pus accumulates under tension and causes throbbing pain.
The pus is not absorbed rapidly by the body and therefore, once pus is formed it should be evacuated, followed by healing of the abscess by granulation tissue. If the pus is not evacuated, the abscess becomes chronic and the pus becomes thickened or inspissated.
The abscess is formed of:
a) Central necrotic tissue surrounded by abscess cavity which contains fluid pus.
b) This is surrounded by an area of living devitalized tissue called pyogenic membrane which shows the vascular phenomenon.
So for an abscess to occur there must be:
1- A big dose of pyogenic organisms causing necrosis of tissues.
2- Localization of infection by fibrin threads.
3- Liquefaction of necrotic tissue and the formation of the fluid pus (by proteolytic enzymes released from pus cells)
The fluid pus:
1- It is thick alkaline fluid which does not clot because fibrin is digested by enzymes.
2- It is usually yellow in color
3- It is usually odorless but become offensive if the
causative organism is E.coli
The fluid pus is formed of:
1- Liquefied necrotic tissue.
2- Living and dead organisms.
3- Pus cells (dead neutrophils).
4- Fluid part of inflammatory exudates.
Sites of abscess: any where in the body e.g. subcutaneous tissues, perianal region, lung, liver, spleen, brain, kidney, breast. … etc
Other types of localized suppurative inflammation:
2. Furuncle or boil:
It is an abscess in relation to hair follicles or sebaceous gland. It is caused by staphylococci e.g. acne.
3. Carbuncle:
This is a large suppurative lesion which develops usually in diabetic patients because of their low resistance to infection. The commonest site is the back of the neck, scalp, and buttocks because the subcutaneous tissue in this area is tough and is divided into compartments by fibrous septa. The suppurative lesion is made of multiple cavities which
communicate with each other and open through multiple points in the skin
Fate of an abscess: 1. If evacuated
Healing process occurs or complicated by failure in healing process results in (ulcer, sinus or fistula.)
Ulcer: it means discontinuation of surface epithelium.
Fistula: means a tract of septic granulation tissue which connects two cavities together or a cavity to the outside and has a free ends.
Types of fistula:
a. Congenital fistula: as the thyroglossal fistula.
b. Inflammatory fistula: as the anal fistula (which
connects a cavity of peri-rectal abscess with the rectal
cavity) and the appendicular fistula (which connects the
infected appendix with the anterior abdominal wall).
c. Malignant fistula: as a complication of malignant
tumors.
1. In females: (cancer cervix may cause vesico-vaginal fistula or recto-vaginal fistula).
2. In males: (cancer urinary bladder may result in rectovesical fistula).
Sinus: means a tract of septic granulation tissue which connects a cavity to the outside and has a blind end.
Examples of sinus: are those sinuses occurring in cases of chronic suppurative osteomyelitis, tuberculosis of cervical lymph nodes, and tuberculosis epidedymitis.
2. if not evacuated:
a. Becomes chronic
b. Undergoes pathological calcification.
Why an abscess should be evacuated?
1. To relief the pain and pressure.
2. To help elimination of bacteria.
3. To reduce abscess cavity and to allow process of healing by fibrosis.
4. Prevent complications.
So the complications of abscess are:
1. Chronic abscess.
2. Chronic ulcer.
3. Lymphangitis and lymphadenitis.
4. Septicemia and pyaemia.
B) Diffuse suppurative inflammation or cellulitis
This kind of inflammation is caused by streptococci which produce:
1. Streptokinase which liquefies fibrin.
2. Hyaluronidase which liquefies the ground substance of fibrous tissue.
These enzymes allow the streptococci to spread very rapidly
in the infected tissue.
Sites:
a. Lax subcutaneous tissue: as in the orbit, scrotum, pelvis
and mediastinum. Here it is called cellulitis.
b. Mucous membrane: as the appendix, where it is called
phlegmonous inflammation.
Pathological changes differ from those of abscess in several ways:
1. Extensive necrosis.
2. Pus forms slowly and may contain many red cells (The capillaries are destroyed by toxins)
3. Rapid spread in tissues and lymphatics.
Complications of diffuse suppurative inflammation:
a. Local spread leads to lymphangitis and lymphadenitis
b. Spread by blood leads to toxemia, septicemia and
pyemia.
Fate of acute inflammation: It depends on two factors:
1. The amount of tissue damage.
2. Whether or not the causative reagent remains in the body.
The common termination of acute inflammation:
I. Resolution: subsidence of inflammatory changes and
return of the tissue to normal. This occurs when the tissue
damage is slight. The damage is reversible when the
causative agent is overcomed by the defensive mechanism
of the body.
II. Progress to suppuration: this occurs when tissue damage is severe as in infection by pyogenic bacteria or by strong chemicals.
III. Chronicity: this occurs when the body cannot get rid of the causative agent, so it remains in the body and continue to produce damage. This is usually accompanied by the formation of granulation tissue and fibrosis.
IV. Spread: occurs when defensive mechanisms are not enough to destroy causative agent, which will grow rapidly.
Spread of inflammation may take place by the following
ways:
a. Spread by natural spaces such as:
Serous membranes as peritoneum, pleura, pericardium, and synovial membranes e.g. perforation of acute suppurative appendicitis leads to acute suppurative peritonitis.
b. Spread by natural passages: as bronchi,
ureters, and G.I.T.
c. Spread by lymphatics: to the draining lymph nodes
(lymphadenitis) from which the organism may enter the
blood stream.
d. Spread by blood stream: causes bacteremia, septicemia,
or pyemia depending on the dose of organisms and way of
entrance.
TYPES OF ACUTE INFLAMMATION
Depending on the type of irritant on one hand and the site of inflammation, the final picture of inflammation is varied and consequently the following types of inflammation are recognized:
I. Non-suppurative inflammations:
1. Catarrhal inflammation.
2. Fibrinous inflammation which may be serous or serofibrinous.
3. Membranous inflammation.
4. Hemorrhagic inflammation.
5. Allergic inflammation.
II. Suppurative inflammations:
a. Localized suppurative inflammation: (abscess, boil,
and carbuncle).
b. Diffuse suppurative inflammation or cellulitis.
Non-suppurative inflammations:
1- Catarrhal inflammation: it is a mild type of acute
inflammation affecting the mucous membrane such as:
■ Inflammation of upper respiratory tract: nose, larynx, and trachea.
■ Inflammation of gastro-intestinal tract: stomach, appendix, and gall bladder.
Pathogenesis: the mucus membrane becomes red, congested, hot, swollen, and dry. This is followed by the appearance of watery discharge which lasts2-3 days, and then the discharge becomes thick and mucoid (because the mucous cells secrete more mucin. Microscopically:
■ The cells of mucous membrane are swollen with accumulation of excessive mucin i.e. mucoid degeneration.
■ The submucosa is swollen, edematous, and contains few polymorphs and numerous thin walled blood vessels filled with blood.
Fate:
■ Good fate: complete recovery is the rule (i.e. after few days, the mucous membrane returns back to normal.
H If secondary bacterial infection occurs, the discharge becomes mucopurulent.
2- Fibrinous inflammation: Sites:
■ Inflammation of serous membranes as pericardium, pleura, and peritoneum.
■ The alveoli of the lung in a disease known as acute lobar pneumonia.
Pathogenesis:
■ The flat endothelial cells become swollen then some cells are necrosed.
■ In the submucosa there are numerous thin walled dilated blood vessels, neutrophils, and edema fluid.
■ The inflammatory exudate comes out to the surface. It is rich in fibrinogen which is deposited as irregular fibrin network on the surface of serous membrane.
■ The serous membrane looks opaque, thick and irregular instead of being glistening, thin and smooth, this is described as (bread and butter appearance). If the exudate is formed mainly of fibrin, it is called dry fibrinous inflammation.
Effects of fibrinous inflammation:
In dry fibrinous inflammation, due to irritation of the sensitive parietal layer, pain is felt. Audible sound is also heard on auscultation called friction rub. Pain and rub are absent in the serofibrinous type
3- Membranous inflammation or (pseudomembranous or diphtheritic): it is a severe type of inflammation affecting mucous membrane in two main diseases which are diphtheria and bacillary dysentery. Pathogenesis:
■ The organism settles in the mucous membrane producing powerful exotoxin which causes necrosis of the superficial part of the mucosa.
■ The submucosa shows numerous thin walled dilated blood vessels, neutrophils and edema fluid.
■ The inflammatory exudate rich in fibrin passes to the outside and becomes mixed with the necrotic tissue forming a paste which spreads on the surface forming a false or pseudomembrane.
■ The false membrane is formed of (necrotic tissue, fibrin threads, dead and living organisms, neutrophils, and RBC’s). By the naked eye it appears dirty grayish in color. It is loosely adherent to the underlying submucosa by the fibrin threads, and if it is removed, it leaves a bleeding raw surface with superficial ulcers.
Effects of membranous inflammation:
This type of inflammation is often accompanied by severe toxemia due to absorption of large amount of toxins in the circulation causing severe generalized edema. ,
4- Allergic inflammation: this type of inflammation is
caused by antigen-antibody reaction. It is characterized by:
a. Excessive edema fluid.
b. Eosinophils are numerous in the tissue as well as
blood.
c. Necrosis.
■ Examples of allergic inflammation are: some skin disease as eczema (allergic dermatitis), urticaria, and allergic rhinitis.
5- Hemorrhagic inflammation: This type of inflammation
is characterized by the presence of large number of R.B.Cs
in the inflammatory exudate due to destruction of the walls
of blood vessels. This type is seen in cases of fevers as
typhus and small pox. In this condition the inflammatory
area looks hemorrhagic.
CHRONIC INFLAMMATION
A chronic inflammation may follow acute inflammation or may start as chronic inflammation from the beginning when it is caused by a mild infection with a prolonged action, e.g. Tuberculosis.
Types of chronic inflammation: I. Chronic specific inflammations:
These are caused by specific organisms which produces a characteristic histological appearance as occurs in tuberculosis, leprosy and syphilis. In many types of chronic specific inflammation, the chronic inflammatory ceils form tumor like masses and therefore they are sometimes known
as granulomatous inflammation or granuloma. II. Chronic non-specific inflammation:
It is a chronic inflammation caused by different types of organisms which does not produce a characteristic histological appearance.
NB. Chronic inflammation is a type of inflammation in which the inflammatory destruction of tissues goes simultaneous (at the same time) with tissue repair.
CLASSIFICATION OF INFLAMMATION
We can classify inflammation to: Acute, Sub acute and chronic
DIFFERENCES BETWEEN ACUTE AND CHRONIC
INFLAMMATION
| Characters | Acute | Chronic |
| Onset | Rapid | Gradual |
| Duration | Short (3 weeks) | Prolonged (months or years) |
| Cardinal signs of inflammation | Present and evident | Mild or absent |
| Toxemia | Acute toxemia | Chronic toxemia |
| Microscopically: a) Cells | P.N.L
(polymorphs) are the main cells and pus cells. Histiocytes, and lymphocytes appear later on. |
Histiocytes, lymphocytes, plasma cells, giant cells and fibroblasts |
| b) Edema fluid | Present | Slight or absent |
| c) Blood vessels | Numerous, thin walled, dilated and filled with blood. | Less numerous, thick walled and may show endarteritis obliterans. |
Types of inflammatory cells:
A) The acute inflammatory cells: (blood borne cells).
1- Polymorphnuclear leucocytes (neutrophils- PXL):
They are derived from the blood and appear in the area of inflammation to attack, phagocytose and kill the organisms.
2- Pus cells:
If the organisms kill the polymorphs, they will transform into pus cells (dead polymorphs). The pus cells produce proteolytic enzymes which liquefy the necrotic tissues in the area of inflammation.
B) The chronic inflammatory cells:
1- Histiocytes or tissue macrophages:
They are members of the reticuloendothelial system but some may come from the blood monocytes. They appear in the late stage in acute inflammation and in most types of chronic inflammation. They phagocytose the necrotic tissues and debris in order to prepare the inflamed area for the process of repair.
2- Lymphocytes:
They are of two types, T lymphocytes which produce cytokines in acute inflammation and B lymphocyte which upon antigenic stimulation transform into plasma cells which produce antibodies.
3- Eosinophils:
It is a type of white blood cells which appear in large number in allergic and parasitic inflammations.
4- Giant cells:
They are large cells with multiple nuclei. They phagocytose the large foreign particles.
5- Fibroblasts:
They are cells which produce collagen fibers and lead to repair by fibrosis in chronic inflammation. It also plays a role in the process of repair and healing.
INFLAMMATION
Definition: it is the reaction of living tissue against an irritant by which the local defensive mechanism of the body comes outside blood vessels to attack the irritant to prevent more damage of tissues.
Nomenclature: suffix- ITIS is usually added to the name of the inflamed tissue (dermatitis, gastritis, myocarditis, and appendicitis… etc)
Causes of inflammation: (these are referred to as irritants) the causes of inflammation could be:
I. living agents
■ Bacteria and its toxins (the commonest cause).
■ Viruses, parasites, and some fungi.
II. Non living agents:
Physical agents: (excessive heat or cold), radiation (infra
red, ultraviolet and ionization)
Chemical agents: (strong acids and alkalis)
Mechanical agents: (wounds, fracture, and crushing injuries)
Injury due to antigen-antibody reaction (hypersensitivity)
Effects of the irritant:
If the irritant is strong it will lead to death of the tissues (necrosis)
If the irritant is mild or moderate it will lead to either:
a. Degeneration of cells
b. Inflammation with its local and general effects.
Effects of inflammation:
When the irritant reaches the tissues it causes injury to the cells resulting in the release of various chemicals substances called (mediators) these mediators initiate either local or general effects.
Effects of inflammation
a. Local effects.
b. General effects.
A. Local effects of inflammation:
These are in the form of vascular changes (the vascular phenomenon or vascular response).
The vascular phenomena:
It is a very important feature of inflammation especially the acute type. It takes place in the small blood vessels by which an important defensive mechanism, namely the inflammatory exudate comes out from inside the blood vessels to the area of inflammation in order to attack the irritant.
This inflammatory exudate is formed of two parts:
The vascular phenomenon takes place in the following steps:
a. Liberation of histamine like substance acting directly on the vessel walls
b. Reflex stimulation of the vasodilator and paralysis of the vasoconstrictor nerve endings.
3. Slowing of the circulation (stasis) begins after few
hours and it is due to:
a. Vasodilatation of the vessels.
b. haemoconcentration of blood due to escape of
plasma to the outside.
c. Swelling of the endothelial cells lining the
vessels.
4. Escape of the plasma to the zone of inflammation to
form the fluid part of the inflammatory exudate. This
escape may be due to:
a. The increase in capillary permeability which is
due to histamine like substance, and it is
maintained by the chemical substance formed
at the site of inflammation.
b. Increase arterial hydrostatic pressure due to
active hyperemia
c. Increase osmotic pressure outside the vessels
due to breakdown of the protein molecules.
This results in widening of gaps between the endothelial cells allowing plasma to escape to the interstitial spaces. Exudation of fluid starts within 10 minutes to several hours from the injury.
5. Pavementation or margination of leucocytes:
Normally the cellular part of the blood is present in the
center taking an axial zone, surrounded by the plasma as a
peripheral zone. This arrangement is governed by the
normal velocity of the circulation. In inflammation due to
slowing of circulation, the leucocytes leave the axial zone
and adhere to the inner endothelial wall of the capillaries. This is known as pavementation or margination which facilitates migration of leucocytes.
So as a result of the vascular phenomenon we get the inflammatory exudates outside the blood vessels. The inflammatory exudate is formed of two parts:
a. Cellular part
b. fluid part
Characters of inflammatory fluid exudate:
Function of inflammatory exudate:
A. Cellular part (mainly neutrophils: P.N.L)
B. Fluid part (plasma)
Functions of the cellular part (P.N.L):
The polymorph nuclear leucocytes attack, phagocytose and kill the organisms by the action of their enzymes i.e. microphages. This is helped by opsonins. Later on phagocytosis occurs by the macrophages. Some neutrophils will die; the dead neutrophils are called pus cells which release proteolytic enzymes that liquify the necrotic tissues.
Function of the fluid part (plasma):
■ Antitoxin to antagonize the bacterial toxins.
■ Opsonins: The antibody makes a coat around the bacteria to help their phagocytosis.
■ Agglutinins: The antibody causes clumping of bacteria together to limit their spread.
■ Specific antibodies causing immunity against certain specific diseases.
Chemotaxis: it means chemical attraction of polymorphs. The movement of polymorphs in the tissue spaces is directed under the influence of bacterial toxins, activated complement, and products of necrotic tissue towards the bacteria. These are called chemotactic substances. N.B. complement is a group of plasma proteins (enzymes) which on activation acts as chemotactic agents, help phagocytosis, and destroy bacteria.
Phagocytosis: it is engulfing the foreign body as bacteria and debris by polymorphs (leucocytes). There are 2 phagocytes cells.
■ Neutrophils.
■ Macrophages (they are derived from monocytes of blood and from tissue histiocytes).
The aim of phagocytosis is to clean and clear the area of inflammation or tissue damage to prepare the tissue for repair. The process of phagocytosis is facilitated by presence of opsonins, complement, fibrin and high temperature.
The cardinal signs of inflammation
B. General effects of inflammation
1. Fever:
Results from the effect of products released from necrotic cells or from leucocytes (under effect of bacterial endotoxin) which act on heat centers. Fever suppresses the growth of some bacteria but when it is severe it may cause more harm to the body.
2. Changes in the blood cells:
A. Changes in whit blood cells:
a. Leucocytosis or increased number of leucocytes. It occurs
in certain types of inflammation and this maybe due to the
leucocyte promoting factor produced locally at the site of
infection but acting on the bone marrow. (The normal
leucocytic count is 5,000 -10,000 c.mm).
■ The neutrophils -> increase in pyogenic or suppurative inflammation.
■ The eosinophils -> increase in parasitic infections and in allergic lesion
■ The lymphocytes -> increase in chronic infections and in viral infections
■ The monocytes increase in typhoid fever, malaria and influenza.
b. Leucopenia or decreased number of leucocytes. It occurs
in typhoid fever, malaria, and some viral inflammation.
B. Changes in the red blood cells: some degree of anemia may develop and may be due to:
■ Toxic depression of the bone marrow.
■ Heamolysis of the RBC’s which occurs in malaria or may be due to the hemolysins produced by heamolytic streptococci.
3. Changes in the organs:
a. Hyperplasia of the reticulo-endothial cells: this
hyperplasia is part of generalized defensive mechanism
of the body and is linked to the development of
immunity.
b. Degeneration of parenchymatous organs due to toxic
effects.
c. Toxemia, septicemia and pyemia.
Acute inflammation is not always protective mechanisms but sometimes it is harmful. So the effects of inflammation may be:
A) Beneficial effects:
It results from the inflammatory exudates and its useful function (function of its cellular part and fluid part).
B) Harmful effects:
1- Swelling of acutely inflamed tissues may lead to serious effects as:
- In acute laryngitis, the lumen of the larynx may be reduced leading to suffocation.
- In inflammation of the brain i.e. encephalitis and meningitis, the inflammatory exudates may leads to increase intracranial tension.
2- Healing by fibrosis may affect the hollow organs and heart valves leading to obstructive manifestation.
3- Sensitivity against certain inhaled antigens may lead to acute conjunctivitis and rhinitis
Chemical mediators of inflammation:
these are chemical substances produced locally at the area of acute inflammation probably from the damaged tissues. They are responsible for the vasodilatation and vascular phenomenon.
Chemical mediators of acute inflammation
| Chemical mediators | Producing cells | Effects |
|
Histamine & serotonin |
Mast cells | Vasodilatation |
|
Prostaglandins |
Mast cells | Vasodilatation & edema |
|
Cytokines |
Macrophage & activated lymphocytes | Neutrophilia |
|
Complement components |
Vasodilatation | |
|
Platelet activating factor |
Mast cells | Platelet aggregation and release |
Types of inflammation:
Acute:
- Non suppurative:
1- Catarrhal inflammation
2- Fibrinous inflammation
3- Membranous inflammation
4- Allergic inflammation
5- Hemorrhagic inflammation
- Suppurative inflammation:
1- Localized suppurative inflammation e.g.: abscess, boil and carbuncle.
2- Diffuse suppurative inflammation e.g.: cellulitis Chronic:
1- Chronic specific inflammation: granulomas
2- Chronic non specific inflammation
