Pathogenic Microbiology Test 2

Front 1

What is mutualism?

Back 1

It is a case in which both the host and the bacteria benefit.

Front 2

What is commensalism?

Back 2

It is a case in which bacteria benefit and the host in which it resides is uneffected.

Front 3

What is a pathogenic relationship?

Back 3

When a host is harmed and the bacteria benefit. The organism can cause disease.

Front 4

Define virulence.

Back 4

Virulence is the measure of the degree of pathogenicity.

Front 5

What is the difference between a primary pathogen and an opportunistic pathogen?

Back 5

A primary pathogen causes disease in an uncompromised host, whereas an opportunistic pathogen requires a compromised host in order to cause disease.

Front 6

What are Koch's postulates used for?

Back 6

They are used for identifying whether or not a certain bacteria is associated with disease.

Front 7

What are Koch's four postulates?

Back 7

1. Organisms should be present in diseased hosts but not healthy subjects.

2. Can be isolated and grown in culture.

3. Cause the same disease when re-inoculated into healthy subjects.

4. Organism can be re-isolated from experimental infection.

Front 8

What are the three limits to Koch's postulates?

Back 8

1. Normal flora cause disease (#1)

2. Disease is not curable (#2,3,4)

3. Limited host range (#3)

Front 9

What are the mechanisms of bacterial pathogenesis?

Back 9

Entry, Attachment, Invasion, Evasion, Toxin production.

Front 10

What are the forms of pathogenic entry to a host?

Back 10

Ingestion, Inhalation, Trauma, Needle Stick, Arthropod bite, Sexual transmission.

Front 11

What is required in pathogenic attachment?

Back 11

A receptor and a ligand. The ligand is part of an adhesin.

Front 12

What is an adhesin and what is its pathogenic purpose?

Back 12

An adhesin is a surface molecule that allows bacteria to bind to other molecules. This can be a variety of things, for example, pili, lipoteichoic acid, lipopolysaccharide.

Front 13

What is the ligand?

Back 13

The ligand is a specific part of an adhesin that binds to the receptor.

Front 14

What is the receptor's pathogenic purpose?

Back 14

A receptor is a molecule on the eukaryotic cell that binds to an adhesin.

Front 15

What is tissue tropism?

Back 15

When bacteria pathogenically attach, tissue tropism refers to where in the body the infection occurs.

Front 16

What is species specificity?

Back 16

The host range of a pathogen.

Front 17

How do bacteria attack a host on the extracellular level?

Back 17

They invade by moving through tissue; they secrete enzymes that break down membrane and extracellular matrix proteins.

Front 18

What are neuraminidases and what do they do?

Back 18

They are an protein secreted by a pathogen that attacks on the extracellular level. Neruaminidase breaks down sialic acid, a sugar molecule that is a key component in mucous

Front 19

What is hyaluronidase and what does it do?

Back 19

it is a protein secreted by a pathogen that attacks on the extracellular level. Hyaluronidase breaks down hyaluronic acid, a key component of the extracellular matrix.

Front 20

What are the four types of bacterial evasion from the immune response?

Back 20

Antigenic mimicry, Antigenic cloaking, Antigenic variation, and phase variation.

Front 21

What is antigenic mimicry?

Back 21

Surface components of a bacterium mimic those of the host in an attempt to evade host immune response.

Front 22

What is antigenic cloaking?

Back 22

Binding of host proteins to the surface in an attempt to evade host immune response.

Front 23

What is antigenic variation?

Back 23

Changing antigen composition (like the O-polysaccharide) in an attempt to evade host immune response.

Front 24

What is phase variation?

Back 24

Turning off the expression of a particular molecule in an attempt to evade host immune response (like flagella expression).

Front 25

What are two ways to avoid phagocytic killing?

Back 25

Kill the phagocyte itself, or have a capsule to avoid uptake.

Front 26

How can a bacteria survive within the phagocyte?

Back 26

Prevent fusion with the lysosome, surive within the phagolysosome, or escape the phagosome and live in the cytoplasm.

Front 27

How does endotoxin work?

Back 27

stimulates the innate immune response like fever and inflammation by binding to macrophages and other cells and causing them to release cytokines. Systemic infections (in blood) can cause severe damage and can lead to shock.

Front 28

Where is endotoxin released?

Back 28

From the lipid A component of the LPS (Gram -) upon cell death.

Front 29

Describe the A and B subunits of endotoxins.

Back 29

Active subunit causes damage, and the Binding subunit allows the toxin to bind and enter the cells.

Front 30

Briefly describe superantigens.

Back 30

endotoxins that activate T-cells nonspecifically and MHC, causing T-calls to be activated without requiring an antigen. This can cause release of cytokines and eventually--shock.

Front 31

What are spreading factors and why are they known as such?

Back 31

Hyaluronidase and neruamidase are spreading factors because they aid in the spread of the pathogen.

Front 32

Describe the virulence factor of Pseudomonas aeruginosa.

Back 32

It cannot pass the skin, but it will invade if there is a severe burn or open wound.