The document describes the stages of infectious disease and the mechanisms of inflammation. It discusses the five stages of infection as incubation, prodromal, illness, decline, and convalescence. It then explains the purpose and physiological mechanisms of inflammation, including the five cardinal signs of inflammation. Finally, it differentiates between acute and chronic inflammation, noting that acute inflammation involves increased blood flow and leukocyte migration, while chronic inflammation lasts months or years.
2. OBJECTIVES
The objectives of this unit are to;
Describe the stages of an infectious disease after
the point at which the potential pathogen enters the
body.
List systemic manifestation of infectious diseases
Discuss the purpose of inflammation
Describe the physiological mechanism involved in
the production of five cardinal signs of inflammation
Differentiate the hemodynamic and cellular phases
of inflammatory response
Differentiate between chronic and acute
inflammation
3. Infection is a host organism’s response to a
pathogen, or disease-causing substance.
Infectious Disease is an illness caused by harmful
agents (pathogens) that get into body. most
common causes are; viruses, bacteria, fungi and
parasites.
Infectious diseases usually spread from person to
person through contaminated food or water
through bug bites etc.
Some infectious diseases are minor and some are
very serious.
INFECTIOUS DISEASE
4. An infection is an illness caused by a harmful
microscopic organism that invades the body, called a
pathogen, such as a bacteria, virus, parasite, or
fungi.
There are five stages of infection:
Incubation
Prodromal
Illness
Decline
Convalescence
STAGES OF AN INFECTIOUS DISEASE
5. The period between the first exposure to a
pathogen and the first emergence of
symptoms.
During this stage, a person does not show
any signs or symptoms of sickness.
duration varies based on the type of
pathogen.
Incubation can last hours, days, months, or
(rarely) years.
Incubation Stage
6. period after incubation & before the
characteristic symptoms of infection occur.
People can also transmit infections during this
stage.
infectious agent continues replicating, which
triggers the body’s immune response and mild,
nonspecific symptoms. These symptoms can
include:
low-grade fever
fatigue
Prodromal Stage
7. This stage includes the time when a person shows
apparent symptoms of an infectious disease.
The symptoms of infection vary widely
depending on the underlying cause.
In general, people who have an active infection
may experience:
Fever
Fatigue
Headache
Muscle Aches
Swollen Lymph Nodes
Illness or Clinical Stage
8. During this stage, the immune system mounts a
successful defense against the pathogens, and
the number of infectious particles decreases.
Symptoms will gradually improve.
However, a person can develop secondary
infections during this stage if the primary
infection has weakened their immune system.
During this stage, the virus can still transmit to
other people
Decline Stage
9. The final stage of infection is known as
convalescence.
During this stage, symptoms resolve, and a
person can return to their normal functions.
Depending on the severity of the infection,
some people may have permanent damage
even after the infection resolves.
Convalescence Stage
10. Infection typically occurs in five stages.
The incubation stage occurs right after exposure and
before symptoms develop. This stage can range from
hours for some infections to days, weeks, or even years
for other infections.
The next stage is prodromal, which involves mild,
nonspecific symptoms.
During the illness stage, a person shows the
characteristic symptoms of infection, such as a rash in
chickenpox or vomiting due to food poisoning.
The decline stage occurs when the number of
infectious microbes declines and symptoms resolve.
The final stage is convalescence. During this stage,
symptoms disappear, and the body starts to recover.
SUMMARY
11. refers to the collection of signs & symptoms
expressed by the host during the disease course.
also known as the clinical picture, or disease
presentation, and can be characteristic of any
given infectious agent.
In terms of pathophysiology, symptoms are the
outward expression of the struggle between
invading organisms and the retaliatory
inflammatory and immune responses of the
host.
Symptomatology
12. Manifestations of infection may be local (eg, cellulitis,
abscess) or systemic (most often fever).
may be specific & reflect site of infection (e.g.,
diarrhea, rash, convulsions, hemorrhage, &
pneumonia) or non-specific & can be shared by a No.
of diverse infectious diseases such as fever, myalgia,
headache, and lethargy.
Manifestations in a diseased host can be obvious, as in
the case of chickenpox or measles. or covert such as an
increased white blood cell count, may require
laboratory testing to detect.
Systemic Manifestation of Infectious
Diseases
13. Severe, generalized infections may have life-
threatening manifestations (eg, sepsis and septic
shock).
Manifestations may develop in multiple organ
systems.
Accurate recognition and documentation of
symptomatology can aid in the diagnosis of an
infectious disease
Most manifestations resolve with successful
treatment of the underlying infection.
Continue
14. Inflammation is the body's mechanism for coping
with agents that could damage it.
A protective response to rid the body of the cause
of cell injury and the resultant necrotic cells that
cell injury produces.
A set of complex changing responses to tissue
injury primarily caused by toxic chemicals, some
environmental agents, trauma, overuse, or
infection.
Inflammation is a “second-line” defense against
infectious agents.
INFLAMMATION
15. Inflammation involves a wide variety of physiologic
and pathologic responses intended to:
eliminate the initial cause of cell injury
remove the necrotic cells & damaged tissue,
generate new tissue.
accomplishes by destroying, enzymatically digesting,
walling off, or otherwise neutralizing the harmful
agents such astoxins, foreign agents, or infectious
organisms.
Thus, inflammation is intimately interwoven with the
repair processes that replace damaged tissue or fill in
the residual defects with fibrous scar tissue.
PURPOSE OF INFLAMMATION
16. The causes of inflammation are many and varied:
Exogenous causes:
Physical agents
Mechanic agents: fractures, foreign corps, sand, etc.
Thermal agents: burns, freezing
Chemical agents: toxic gases, acids, bases
Biological agents: bacteria, viruses, parasites
Endogenous causes:
Circulation disorders: thrombosis, infarction,
hemorrhage
Enzymes activation – e.g. acute pancreatitis
Metabolic products – uric acid, urea
ETIOLOGY
17. The five cardinal signs of inflammation
1. Rubor (Redness),
2. Tumor (Swelling),
3. Calor (Heat),
4. Dolor (Pain).
5. Functio Laesa (Loss of Function)
FIVE CARDINAL SIGNS OF
INFLAMMATION
18. RUBOR (REDNESS):
caused by active hyperemia after momentary
vasoconstriction due to stress reaction (catecholamines)
related e.g to pain (injury) - dependent on vasoactive
inflammatory mediators, in the developed (end stage)
inflammation
hypoperfusion of the inflamed area can appear due to micro-
thrombotisation of vessels
hyperemia increases delivery (supply) of cells (leukocytes)
to the place of inflammation
PHYSIOLOGICAL MECHANISM IN THE PRODUCTION OF
FIVE CARDINAL SIGNS OF INFLAMMATION
19. TUMOR (SWELLING):
develops because of increased hydrostatic pressure and
increased permeability of vessels (caused by inflammatory
mediators ); besides transudation into the interstitium, active
exudative (secretion) processes also take place (peritoneal
cavity, pericardium, pleural cavity)
CALOR (HEAT):
Increased temperature of the inflamed area due to
hyperemia and increased metabolism
20. DOLOR (PAIN). –
irritation of free neural endings by inflam. mediators -
mainly prostaglandins, substance P, bradykinin
compression of nerves by edema
developing acidosis in the case of thrombotisation of vessels
(in developed, chronic inflam. process)
FUNCTIO LAESA (LOSS OF FUNCTION)
caused by pain and edema - disabling mainly motion -
prevents overload of the involved parts of the body
21. Vascular phase leads to an increase in blood flow
and changes in the small blood vessels of the
microcirculation.
characterized by changes in the small blood vessels at
the site of injury. begins with momentary
vasoconstriction followed rapidly by vasodilation.
Vasodilation involves the arterioles & venules with a
resultant increase in capillary blood flow, causing
heat and redness. (Two Cardinal signs)
This is accompanied by an increase in vascular
permeability with outpouring of protein-rich fluid
(exudate) into the extravascular spaces.
22. The loss of proteins reduces the capillary osmotic
pressure and increases the interstitial osmotic
pressure.
This, coupled with an increase in capillary
pressure, causes a marked outflow of fluid and its
accumulation in the tissue spaces, producing the
swelling, pain, and impaired function (Other
Cardinal signs)
As fluid moves out of the vessels, stagnation of
flow and clotting of blood occur. This aids in
localizing the spread of infectious
microorganisms.
Continue
23. The cellular stage of acute inflammation is
marked by changes in the endothelial cells lining
the vasculature and movement of phagocytic
leukocytes into the area of injury or infection.
Focused on recruitment of leukocytes from blood
release of chemical mediators from tissue cells
(mast cells and macrophages) prepositioned in the
tissues.
The sequence of events in cellular phase includes;
o Leukocyte Margination & adhesion to
endothelium
o Transmigration across the endothelium.
o Chemotaxis
CELLULAR PHASE
24. The cellular phase of acute inflammation
involves delivery of leukocytes, mainly
polymorphonuclear neutrophils (PMNs), to the
site of injury so they can perform their normal
functions of host defense through phagocytosis.
The delivery and activation of leukocytes can be
divided into the following steps:
o endothelial activation, adhesion and
margination,
o transmigration
o chemotaxis.
LEUKOCYTE MARGINATION &
ADHESION TO THE ENDOTHELIUM
25. The recruitment of leukocytes to the precapillary
venules, where they exit the circulation, is facilitated
by the slowing of blood flow and margination along
the vessel surface
Leukocyte adhesion and transmigration from the
vascular space into the extravascular tissue is
facilitated by complementary adhesion molecules
(e.g., selectins, integrins) on the leukocyte and
endothelial surfaces.
After extravasation, leukocytes migrate in the tissues
toward the site of injury by chemotaxis or locomotion
oriented along a chemical gradient.
Continue
27. Once at the sight of injury, the products generated by
tissue injury trigger a number of leukocyte responses,
including phagocytosis and cell killing.
Opsonization of microbes by complement factor C3b
and antibody facilitates recognition by neutrophil C3b
and the antibody Fc receptor.
Receptor activation triggers intracellular signaling and
actin assembly in the neutrophil, leading to formation of
pseudopods that enclose the microbe within a
phagosome.
The phagosome then fuses with an intracellular
lysosome to form a phagolysosome into which
lysosomal enzymes
Oxygen free radicals are released to kill and degrade
the microbe.
LEUKOCYTE ACTIVATION &
PHAGOCYTOSIS
29. SELECTINS :
E-selectin - (cytokine-activated Endothelial cells)
P-selectin - (Preformed and stored in endothelial cells)
L-selectin (expressed on surface of Lymphocytes and
neutrophils)
INTEGRINS:
Activated during the process of loose and transient
adhesions
between the endothelial cells and leucocytes.
IMMUNOGLOBULIN SUPER
FAMILYADHESION
MOLECULE: ICAM-1,2
ADHESION
MOLECULES:
30. Acute inflammation is the early response of the
organism to adverse stimuli. It is acquired by an
increased transport of leukocytes (especially
granulocytes) and plasma from the blood in the
damaged tissues.
In acute inflammation develops the so called “triple
response of Lewis: (1) redness, (2) increased blood
flow, and (3) edema.
The inflammatory response is spread by series of
biochemical events. The immune system, the local
vascular system, and different cells in the damaged
tissue are included in the process.
ACUTE INFLAMMATION
31. The acute inflammation process is initiated by
immune cells, which are already present in the
involved tissue. These are:
Dendritic cells,
Kupffer cells,
Histiocytes,
Resistant macrophages,
Mast cells.
When infections, burns or injuries occur, the
immune cells are subject to activation and release
inflammatory mediators.
Mediators cause clinical signs of inflammation.
ACUTE INFLAMMATION
32. Vasodilatation and the resulting increased blood flow
cause redness and increased temperature.
Increased permeability of the blood vessels leads to
exudation of fluid and plasma proteins into the tissue.
This results in swelling.
Some of the released mediators (e.g. bradykinin) raise
the sensitivity to pain (hyperalgesia).
The mediators also alter blood vessels to allow
migration of leukocytes, primarily macrophages and
neutrophils, out of the blood vessels (extravasation)
into the tissue.
White blood cells migrate along the chemotaxis
gradient created by local cells to reach the site of injury.
ACUTE INFLAMMATION
33. chemicals originate primarily from blood plasma,
white blood cells (basophils, neutrophils, monocytes,
and macrophages), platelets, mast cells, endothelial
cells lining the blood vessels, and damaged tissue
cells.
Histamine, stored in granules of circulating basophils
and mast cells triggers vasodilation and increases
vascular permeability.
Lysosomal compounds, and small proteins in the
complement system, namely C3a and C5a. released
from neutrophils, involved in increasing vascular
permeability
Cytokines secreted by cells involved in inflammation
also have vasoactive and chemotactic properties.
Chemical mediators of inflammation
34. The prostaglandins a group of fatty acids produced by
many types of cells.
increase the effects of other substances that promote
vascular permeability.
affect the aggregation of platelets, which is part of the
clotting process.
associated with pain and fever of inflammation.
The plasma contains 04 interrelated systems of protein -
generate various mediators of inflammation.
1. Activated complement proteins serve as chemotactic
factors for neutrophils, increase vascular permeability, and
stimulate the release of histamine from mast cells. also
adhere to the surface of bacteria, making them easier
targets for phagocytes.
Continue
35. 2. kinin system, is activated by coagulation factor XII,
produces substances that increase vascular
permeability. The most important of the kinins is
bradykinin, which is responsible for much of the pain
and itching experienced with inflammation.
3. Coagulation system converts the plasma protein
fibrinogen into fibrin, which is a major component of
the fluid exudate.
4. Fibrinolytic system contributes to inflammation
primarily through the formation of plasmin, which
breaks down fibrin into products that affect vascular
permeability.
Continue
36. The chronic inflammation is an inflammatory
reaction that lasts for months or years.
Most often acute inflammation precedes the
chronic, but this is not always the case.
The chronic inflammation can be due to:
Prolonged irritation of chemicals,
Foreign particles – dust, surgical thread, etc.,
Infection by microorganisms that cannot be
overcome for a long time by the body –
tuberculosis, syphilis, brucellosis.
CHRONIC INFLAMMATION
37. The following immune cells are involved in the
chronic inflammation process:
Macrophages,
Neutrophils,
Lymphocytes.
Depending on the body’s response, the chronic
inflammation is:
Granulomatous inflammation,
Non-granulomatous inflammation.
The aim of the chronic inflammation is to limit and
remove the agent, which cannot be removed by
acute response (acute inflammation). Restriction
and removal of the agent depend on the reactivity of
the immune system.
Chronic Inflammation
38. Acute inflammation is of relatively short duration,
lasting from a few minutes to several days, and is
characterized by the exudation of fluid and plasma
components and emigration of leukocytes,
predominantly neutrophils, into the extravascular
tissues.
Chronic inflammation is of a longer duration,
lasting for days to years, and is associated with the
presence of lymphocytes and macrophages,
proliferation of blood vessels, fibrosis, and tissue
necrosis.
Chronic Versus acute inflammation
39. FEATURE ACUTE CHRONIC
Onset Fast
Minutes or hours
Slow
Days or months
Cellular infiltrate Mainly neutrophils
Also have
macrophage
Monocytes/
macrophages &
lymphocytes/
plasma cells,
fibroblasts, giant
cells
Tissue injury,
fibrosis
Usually mild and
self-limiting
Often severe and
progressive
Local & systemic
signs
prominent Less prominent;
may be subtle
DIFFERENCES BETWEEN ACUTE &
CHRONIC INFLAMMATION
