M2-C3-L10 --> Bacterial Pathogenesis Ii

Front 1

Adhesion:

- describe
- reversibility
- bonding

Back 1

Interaction between pathogen adhesins and host cell receptors

Irreversible

Non-covalent

Front 2

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

Back 2

via transcriptional regulation mechanisms

environmental (host) signals.

Front 3

Give two ways that regulation of virulence factors can be SPATIAL.

Back 3

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.

Front 4

Show how regulation of virulence factors can be TEMPORAL.

Back 4

Organisms in same tissue site over time will change virulence gene expression.

Front 5

How does a harmless bacteria become a pathogen?

Back 5

Acquisition of virulence factors via horizontal gene transfer.

Front 6

Describe the evolution of a normal flora bacteria to virulent bacteria.

Back 6

Member will acquire virulent factor to become virulent.

Front 7

Describe the CO-evolution of virulent bacteria with host.

Back 7

Upon contact, host experiences devastating disease.

Over time, the devastation decreases, but becomes more chronic.

Front 8

Which toxins can be inactivated to become toxoids?

Back 8

Endotoxin

Front 9

Endotoxin:

- sensitive/resistant to?
- produced by
- toxic amounts
- made of
- released from
- damage to host
- neutralized

Back 9

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.

Front 10

Exotoxin:

- sensitive/resistant to?
- produced by
- toxic amounts
- made of
- released from
- damage to host
- neutralized

Back 10

Sensitive to heat, autoclave, and proteases

Gram positive and gram negative

Low amounts needed

Proteins

Actively secreted from ALIVE bacteria

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

Neutralized by antibodies

Front 11

Endotoxins are made primarily from what part of Gram negative bacteria?

Back 11

LPS

Front 12

NAD+ components. x3

Back 12

Nicotinamide

ADP

Ribose

Front 13

AB toxins of gram neg. and pos.:

- A subunit does what
- B subunit does what

Back 13

Enzyme activity

Binding and delivery of toxins

Front 14

What is a common enzyme activity of AB toxins?

Back 14

ADP-ribosyltransferase activity

Front 15

Describe the ribosyltransferase activity.

Back 15

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.

Front 16

Cholera Toxin:

- what type of classic example?
- mechanism

Back 16

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.

Front 17

What are hemolysins?

Back 17

Toxins that break down RBC's by "punching" holes in them.

Front 18

What is the difference between alpha and beta hemolysins?

Back 18

Alpha (greenish hue)
Partial breakdown of RBC's

Beta (Clear zone)
Complete breakdown of RBC's

Front 19

How can bacteria use ECM as a self-benefit?

Back 19

By destroying ECM, it will aid in its ability to spread.

Front 20

Hemagglutinins:

- what is it?
- forms what in test tubes?

Back 20

bacteria with adhesins that bind to RBC receptors

complex lattices

Front 21

Pathogenicity island:

- what is it
- properties x8

Back 21

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

Front 22

List and explain the two different ways bacteria can get the iron they need.

Back 22

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.

Front 23

Describe the bacterial defense mechanism known as Phase Variation.

Back 23

Random ON/OFF switching of gene expression, resulting in presence and absence of antigen on surface.

Front 24

Describe the bacterial defense mechanism known as Antigenic Variation.

Back 24

Producing different antigenic proteins at varying times

Front 25

How can bacteria take advantage of the Fc portion of IgG?

Which bacteria does this? x2

Back 25

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

Front 26

Numerous musocal pathogens synthesize what as a defense mechanism against antibodies?

Back 26

IgA proteases

Front 27

Capsules provide protection for bacteria against what cell?

How does this work?

Back 27

Phagocytic cells

Inhibits receptors of phagocytic cells from binding to bacteria.

Front 28

Superantigens:

- bind to where of what cell?
- triggers what effect?

Back 28

V-beta portion of T-lymphocytes

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

Front 29

Salmonella:

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

Back 29

Facultative Intracellular Parasite

Gram NEGATIVE ROD

Typhoid fever + Diarrhea

Type III secretion system
2 PAI's

M-cells

Front 30

Shigella:

- Gram what?
- symptoms x2

Back 30

Gram Negative Rod

Diarrhea & Bloody Stools

Front 31

How does Shigella overcome the fact that it has no flagella for movement?

Back 31

After infection, spreads cell to cell (never goes outside of cell) via

Actin Comet Tail Propulsion

Front 32

What is Actin Comet Tail Propulsion?

Back 32

Movement by polymerizing actin

Front 33

What is the pathogenesis of Listeria?

Back 33

Actin Comet Tail Pathogenesis