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INFECTION
Contents
OUTLINE THE PATHOGENESIS OF INFECTION, ITS EFFECTS ON THE HOST AND THE ROLE OF HOST
FACTORS IN THE DEVELOPMENT OF DISEASE ...................................................................................... 1
Step 1  External Barriers to infection ........................................................................................ 2
Step 2  Spread ............................................................................................................................. 3
Step 3  Evasion of Host Defences at many stages ....................................................................... 4
Step 4  Damage ........................................................................................................................... 6
Step 5  Resolution ........................................................................................................................ 6
EXPLAIN HOW BACTERIA SPREAD BOTH WITHIN A HOST AND BETWEEN HOSTS ................................. 8
REFERENCES.................................................................................................................................... 8
OUTLINE THE PATHOGENESIS OF INFECTION, ITS EFFECTS ON THE HOST AND THE
ROLE OF HOST FACTORS IN THE DEVELOPMENT OF DISEASE
Steps involved in pathogenesis of infection:
i.
Access & Entry – Acquisition, colonisation, penetration
A pathogen must overcome the body’s external defences:
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ii.
Skin e.g. skin secretions (sweat, sebum etc), keratin (protection against bacterial enzymes)
Natural flora providing competition for space and nutrients
Shedding of epithelia
Mucociliary clearance from airways
Spread – Local & Systemic Transmission
A pathogen must immediately overcome local defences. This includes the evasion of the innate immune
system.
iii.
Evasion of Host Defences at many stages
Evasion of host defences. Includes previously described barrier defences of the host, other defences include:
 Innate immunity: Complement and physical barriers.
 Acquired immunity: T- cell mediated.
iv.
Damage – Direct effects of the pathogen, and those secondary to the host response of the
process
A pathogen is then shed from body (exit). Pathogens can be spread between hosts, e.g. passing through the
gastrointestinal tract, droplet spread from the respiratory system, direct spread from the urogenital system.
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v.
Resolution – Activation of the Innate & Acquired Immune Response ± Medical
Treatment
As a result of being infected with a pathogen, the acquired immune response will develop specificity to
recognise if the same pathogen invades the body a second time. This way, a person will not be diseased from
the same pathogen a second time.
Basic overview of immunity
Step 1  External Barriers to infection
External barriers
An invading microorganism initially encounters ‘external’ defences, such as enzymes in secretions
that can damage or destroy microorganisms (e.g. lysozyme in saliva and tears, low pH in the stomach,
sticky mucus on many surfaces, and the presence in the gut and genital tract of normal bacterial flora
that are able to prevent the growth of pathogenic organisms
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Step 2  Spread
Pathogens can be transmitted both locally and systemically.
mechanisms are required. They are characterised by;
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To combat this, innate defence
Rapid, first line of defence against infection
Non-specific (do not distinguish between different pathogens)
Always present at low levels
May be rapidly activated early in an infection or after tissue damage
They slow or prevent the development of infections during the several days that it takes for
the acquired immune system to develop a specific response
A body’s defence system distinguishes certain characteristic molecules on the surface of some
invaders, called pathogen-associated molecular patterns (PAMPs), which acts as flags to identify
bacteria as opposed to the eukaryotic host cells.
If a pathogen passes the initial external defences, internal non-specific defences come into play.
Activation of the complement cascade has three main consequences:
1.
Induction of local inflammation, increasing vascular permeability at the sites of infection and
attracting phagocytes to sites where complement is bound
2. Facilitation of the engulfment by phagocytic cells of microbes or cells with complement
bound to them
3. Lysis of cells and damage to bacteria with complement bound to their surface (by ‘punching’
holes through the cell membrane)
The inflammatory response
When the external barriers are breached, resulting in injury and the introduction of microorganisms,
an integrated, non-specific response called the inflammatory response occurs. Chemicals released in
the damaged or infected tissue, such as histamine released from stimulated mast cells and cytokines
initiate a series of local changes including;
1. Widening of capillaries, causing an increased blood flow to the area
2. Increased permeability of the capillaries, causing a release of plasma into the surrounding
tissue
3. Attraction of phagocytes, monocytes (which develop into macrophages) and neutrophils to
the site and their migration into the surrounding tissue
This results in:
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Redness
Swelling
Pain
Increased warmth all at the side of the affected area.
The phagocytes attracted to the area attack and engulf bacteria and remove cell debris. Antibodies
and complement move to the site and lead to the development of the specific immune response.
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Step 3  Evasion of Host Defences at many stages
Adaptive Immune System
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Takes time to develop
Therefore, important in recovery from disease more than preventing infection initially
Specific response. E.g.: distinguishes between different infecting microorganisms or strains of
the same microorganisms.
Has immunological memory
o Primary response  person vaccinated against disease, immune system recognises it
o Secondary response  person comes contact with disease again, system recognises
disease and is more efficient in preventing infection second time around
Cells involved in specific acquired immunity
There are two distinct kinds of immune response that are usually effective against different kinds of
microorganisms: a cellular response (mediated by T cells type of acquired immunity is achieved
through the formation of large numbers of activated T lymphocytes that are specifically crafted in the
lymph nodes to destroy the foreign agent.), and a humoral response (in serum – mediated by
antibodies produced by B lymphocytes - the body develops circulating antibodies, which are globulin
molecules in the blood plasma that are capable of attacking the invading agent.)
Cells involved in immune response:
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Cells of immune response in more detail:
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Step 4  Damage
Damage results from direct effects of the pathogen and those secondary to the host response of the
process. Pathogens can be spread from various means, namely through
i.
ii.
iii.
iv.
v.
vi.
Contact (eg. Touching surfaces contaminated by Hep B)
Inhalation (eg. Breathing in airborne droplets infected with Step. Pneumoniae) –
Horizontal
Ingestion (eg. Eating food contaminated with Salmonella)
Inoculation (eg. Transmission of Hep C from sharing needles)
Transplacental (eg. Tetratogens, like Leukaemia, crossing the placenta from mother to
child) – Vertical Transmission
Vectors (eg. Mosquitoes carrying Malaria)
Step 5  Resolution
Activation of the Innate & Acquired Immune Response ± Medical Treatment

If a person is exposed to the same pathogen a second time, the acquired immune response will
be activated to enhance the immune defences of the body. This can be achieved with
vaccination or from being exposed to the pathogen and recovering from infection
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Clinical features of acute inflammation
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EXPLAIN HOW BACTERIA SPREAD BOTH WITHIN A HOST AND BETWEEN HOSTS
Bacteria spread within a host the following ways:
1. The ability to use motility and other means to contact host cells and disseminate within a host.
2. The ability to adhere to host cells and resist physical removal.
3. The ability to invade host cells.
4. The ability to compete for iron and other nutrients.
5. The ability to resist innate immune defences such as phagocytosis and complement.
6. The ability to evade adaptive immune defences.
Bacteria spread between hosts the following ways:
Some bacteria produce adhesion molecules called invasins that activate the host cell's cytoskeletal
machinery enabling bacterial entry into the cell by phagocytosis. Advantages of entering a human cell
include:
a) Providing the bacterium with a ready supply of nutrients
b) Protecting the bacteria from complement, antibodies, and other body defence molecules
In addition, some pathogenic bacteria:
a) Invade phagocytic cells, neutralize their killing ability, and turn them into a safe haven for
bacterial replication
b) Kill phagocytic dendritic cells once they are engulfed and prevent those dendritic cells from
activating the T4-lymphocytes and T8-lymphocytes required for adaptive immunity
REFERENCES
Abbas, A & Litchtman, A. (2011). Basic Immunology. Philadelphia: Elsevier.
Colledge, N., Walker, B.& Ralston, S. (2010). Davidson’s Principles and Practices of Medicine.
Philadelphia: Churchill Livingstone.
Knox B, Ladiges, P., Evans, B. & Saint, R (2007). Biology – An Australian Focus. Australia: McGraw
Hill.
Sherwood, L. (2004). Human Physiology: From Cells to Systems (5th Edition). Australia: Thompson.
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