4-Pathogenesis & Virulence Lecture

Pathogenesis and
virulence
Dr/ Ayman Alashkar

MD parasitology and immunology
Assistant professor at UBCOM
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Our Objective
By the successful completion of this
presentation, you are expected to:
Specific Learning
• Define pathogenesis and virulence.

Outcomes
• Name the methods of transmission of

infection.
• Describe the process of infection
• Explain the mechanism of disease
production by bacteria.
• List the bacterial virulence factors.
• Give examples of instances where bacterial
virulence factors play important role in
virulence, antibiotic susceptibility and host
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defense
Bacterial virulence factors
A. The ability to adhere to host cells & resist
physical removal:
Fimbriae (Pili)
Enable some organisms to adhere to receptor on target
host cells.
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B. Invasion:
• Invasiveness ➔is the ability of the organism
to enter host's tissues, multiply there and
spread to other tissues.
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C. The ability to resist host immune defense
and unfavourable environmental conditions:
a. Capsule: resist phagocytosis e.g. Streptococcus pneumoniae

polysaccharide capsule.
b. Immunoglobulin A protease ➔ degrades IgA ➔allowing the
organisms to adhere to mm, e.g. S. pneumoniae.
c. Leukocidin ➔destroy both PNL and MΦ e.g. Staph aureus.
d. Cell wall proteins of Gram +ve cocci, such as
• Protein A of Staph aureus: bind to the Fc portion of Ab ➔
prevent opsonization.
e. Coagulase Enzyme: Accelerates the formation of a fibrin clot
➔protect the bacteria from phagocytosis, e.g. Staph aureus.
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f. Bacterial Spores:
• Spores are highly resistant resting (or dormant) stage
of the bacteria formed in unfavorable environmental
conditions as a result of the depletion of exogenous
nutrients.
• Sporicidal agents: Spores are highly resistant. Only
limited sterilization methods are available to kill the
spores
• Used as indicator for proper sterilization.
○○ Spores of Geobacillus stearothermophilus are
used as sterilization control for autoclave.
○○ Used as agents of bioterrorism; e.g. Spores of
Bacillus anthracis in the 2001 USA attack.
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D. Damage to host cells by inflammatory
response or bacterial toxins:
A) Specific HIR and CMIR (inflammatory
response): the presence of microbial antigen
elicits humoral and cell-mediated immunity
resulting in immunopathology which may
persist even after the infection is eliminated.
B) Bacteria can damage the host tissues by:
1) Endotoxin.
2) Exotoxins.
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Exotoxins
b. Membrane
a. A-B toxins
Disrupting c. Super Ag
Toxins
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a. A-B toxins
• These toxins interfere with cell
metabolism.
• Each is formed of 2 portions:
• Portion B: Binds to specific host
cell receptors.
• Portion A: Active enzymatic
portion of the
toxin➔translocated into host
cells after binding of B portion.
• Examples:
9 Diphtheria exotoxin.
b. Membrane Disrupting Toxins (Cytolytic
enzymes)
• Cause lyses host cells by disrupting the plasma
membrane.
• These toxins are general cytotoxins because
they can affect any host cell.
• Example: hemolysin production by
Staphylococcus aureus disrupt cell membrane
of RBCs
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c. Superantigens
• Non-specific activation of very large numbers
of lymphocytes ➔ release of large amount of
IL-2 & other cytokines➔ shock.
• Examples: Toxic shock syndrome toxin-1
(TSST-1) of Staph aureus.
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Exotoxins Endotoxins
1) Source Secreted by both Gram +ve Integral part of cell wall of Gram -ve
(mainly) and Gram -ve organisms. organisms.
2) Chemistry Protein in nature (polypeptide). LPS.
3) Mechanism Diffusible, secreted by living cells. Non diffusible, released on cell lysis.
of release
4) Toxicity Very high toxicity. Low toxicity.
5) Antigenicity Highly antigenic stimulate antitoxin Poorly antigenic.
production
6) Effect of Convert it into toxoid (antigenic but No effect. Can not be converted to
formalin non toxigenic). toxoid.
7) Effect of Unstable to temperature above Stable at temperature above 60°C for
heat 60°C, toxicity destroyed rapidly. several hours without loss of toxicity.
8) Specificity Every toxin has specific action. Not specific in action (all give fever
and shock).
9) Fever Do not produce fever in the host. Produce fever in the host through
release of interleukin-1 from
12 macrophages.
Chain of infection
• 1. Reservoir ➔a place in which an infectious
agent can survive but may or may not
multiply.
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2. Pattern of transmission
• Communicable diseases: when an infected host can
transmit the infectious agent to another host and
establish infection in that host through different
portal of exits.
• Eg: Influenza and measles move readily from host to
host and thus are contagious.
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Portal of exit
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Non communicable diseases:
• Does not arise through transmission of the
infectious agent from host to host.
• Eg: tetanus, in which Clostridium tetani
endospores from a soiled object enter a cut or
wound. Infected persons do not become a
source of disease to others.
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3. Establishment of infection
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1. Lag Phase: In this phase:
✓ The number of cells present appears to remain constant
although they may increase greatly in size as the cells
adapt to their new environment.
✓ They start to synthesize enzymes and molecules
required for bacteria growth.
✓ It corresponds to incubation period of the disease.
2. Prodromal phase (1-2 days):
✓ The earliest notable symptoms of infection usually
appear as vague feeling of discomfort, such as
headache, muscle aches, fatigue, stomach upset &
general malaise.
2. Exponential Phase (Log phase):
✓ It is the most active phase of bacterial growth.
✓ The number of bacteria increases steadily by time.
✓ This phase continues until the nutrient of the medium is exhausted
or toxic metabolites accumulate. Bacteria are highly susceptible to
antibiotics at this phase.
✓ It corresponds to active phase of the disease.
4. Stationary Phase:
✓ Exhaustion of nutrients and accumulation of toxic products cause
a decrease in the growth.
✓ There is slow loss of cells through their death that is balanced by
formation of new cells through growth and division.
✓ The number of viable bacteria ➔ constant.
✓ It corresponds to active phase of the disease
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5. Decline or Death Phase:
✓ The death rate  and exceeds the
multiplication rate.
✓Due to nutrient exhaustion & accumulation of
toxic products.
✓It corresponds to convalescence phase &
recovery from the disease
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References
• Microbiology: A System Approach BY Marjorie

K Cowan, 4th Edit. Chapter 13, Pages 355-381.
• Review of microbiology and immunology
pages: 9-14
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Pathogenesis and

Dr/ Ayman Alashkar

• Define pathogenesis and virulence.

• Name the methods of transmission of

a. Capsule: resist phagocytosis e.g. Streptococcus pneumoniae

• Microbiology: A System Approach BY Marjorie

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