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33 Cards in this Set

  • Front
  • Back

- describe
- reversibility
- bonding
Interaction between pathogen adhesins and host cell receptors


Bacteria control the expression of virulence factors via __________ in response to __________.
via transcriptional regulation mechanisms

environmental (host) signals.
Give two ways that regulation of virulence factors can be SPATIAL.
1. Multiple niches in human body that are supportive of bacterial growth will provide multiple environmental signals to bacteria.

2. Different sites in the human body may trigger different virulence determinants.
Show how regulation of virulence factors can be TEMPORAL.
Organisms in same tissue site over time will change virulence gene expression.
How does a harmless bacteria become a pathogen?
Acquisition of virulence factors via horizontal gene transfer.
Describe the evolution of a normal flora bacteria to virulent bacteria.
Member will acquire virulent factor to become virulent.
Describe the CO-evolution of virulent bacteria with host.
Upon contact, host experiences devastating disease.

Over time, the devastation decreases, but becomes more chronic.
Which toxins can be inactivated to become toxoids?

- sensitive/resistant to?
- produced by
- toxic amounts
- made of
- released from
- damage to host
- neutralized
Resistant to heat, autoclave, proteases

Gram Negative bacteria only

High amounts needed

Lipids and Carbohydrates

Live (blebs) and dead bacteria

Initiates septic shock cascade

POORLY neutralized by antibodies.

- sensitive/resistant to?
- produced by
- toxic amounts
- made of
- released from
- damage to host
- neutralized
Sensitive to heat, autoclave, and proteases

Gram positive and gram negative

Low amounts needed


Actively secreted from ALIVE bacteria

Damage varies, but damage/kills host cell, as well as stimulate inflammation. Also causes cell tropism

Neutralized by antibodies
Endotoxins are made primarily from what part of Gram negative bacteria?
NAD+ components. x3


AB toxins of gram neg. and pos.:

- A subunit does what
- B subunit does what
Enzyme activity

Binding and delivery of toxins
What is a common enzyme activity of AB toxins?
ADP-ribosyltransferase activity
Describe the ribosyltransferase activity.
This toxin will take a common NAD+ molecule, and

separate the nicotinamide (NAm) from the ADP-ribose.

The ADP-ribose will then attach itself to an activated target protein.

This attachment will make the target protein INACTIVE, thus unable to carry out normal function.
Cholera Toxin:

- what type of classic example?
- mechanism
Classic AB toxin

Normally, ACTIVE G-protein will sequester (inactivate) adenylate cylcase.

Binding of cholera toxin will release A1 subunit.

A1 subunit attaches to active G-protein, making it INACTIVE.

This will activate Adenylate Cyclase which will convert ATP to cAMP.

This will trigger the release of K+, Na+, and HCO3- into the gut lumen.

Massive water follows, leading to voluminous diarrhea.
What are hemolysins?
Toxins that break down RBC's by "punching" holes in them.
What is the difference between alpha and beta hemolysins?
Alpha (greenish hue)
Partial breakdown of RBC's

Beta (Clear zone)
Complete breakdown of RBC's
How can bacteria use ECM as a self-benefit?
By destroying ECM, it will aid in its ability to spread.

- what is it?
- forms what in test tubes?
bacteria with adhesins that bind to RBC receptors

complex lattices
Pathogenicity island:

- what is it
- properties x8
Genomic island formed by horizontal gene transfer.

1. Carriage of virulent genes
2. Association with pathogenic strains
3. Association with tRNA
4. Motility genes present
5. Flanked by direct repeats
6. Instable
7. G-C content differs
8. Size increase
List and explain the two different ways bacteria can get the iron they need.
1. Siderophore mediated iron uptake
Bacteria secretes siderophore which chelates with iron and brings it back to bacteria. Siderophore is recycled.

2. Non-siderophore mediated iron uptake
Bacteria produce receptors on its surface that binds to proteins and steals their iron.
Describe the bacterial defense mechanism known as Phase Variation.
Random ON/OFF switching of gene expression, resulting in presence and absence of antigen on surface.
Describe the bacterial defense mechanism known as Antigenic Variation.
Producing different antigenic proteins at varying times
How can bacteria take advantage of the Fc portion of IgG?

Which bacteria does this? x2
Bacteria can make proteins that bind to Fc, such that the actual antigen binding portions of antibodies can not be used against them.

Staphylococcus Aureus
Streptococcus Pyogenes
Numerous musocal pathogens synthesize what as a defense mechanism against antibodies?
IgA proteases
Capsules provide protection for bacteria against what cell?

How does this work?
Phagocytic cells

Inhibits receptors of phagocytic cells from binding to bacteria.

- bind to where of what cell?
- triggers what effect?
V-beta portion of T-lymphocytes

Massive proliferation of active T-cells that are nonspecific for an antigen, thus useless.

- Intracellular or extracellular?
- Gram what?
- symptoms x2
- Pathogenesis requirements x2
- likes to invade/enter what cell?
Facultative Intracellular Parasite


Typhoid fever + Diarrhea

Type III secretion system
2 PAI's


- Gram what?
- symptoms x2
Gram Negative Rod

Diarrhea & Bloody Stools
How does Shigella overcome the fact that it has no flagella for movement?
After infection, spreads cell to cell (never goes outside of cell) via

Actin Comet Tail Propulsion
What is Actin Comet Tail Propulsion?
Movement by polymerizing actin
What is the pathogenesis of Listeria?
Actin Comet Tail Pathogenesis