Lecture 8 - Colonization Flashcards

1
Q

Describe commensalism.

A

The host is unaffected while the microbe benefits.

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2
Q

Describe parasitism.

A

The host is harmed while the bacteria benefits.

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3
Q

What does symbiosis mean?

A

Living together.

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4
Q

Where can normal microbiota be found on the body?

A
Skin 
Conjunctiva 
Respiratory tract 
Urogenital tract 
GI tract
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5
Q

What type of symbiosis occurs with natural microbiota?

A

Mutalists + Commensals

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6
Q

What are the characteristics of normal microbiota?

A

Stable, polymicrobial communities

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7
Q

What are the benefits of normal microbiota?

A

Can prevent the colonization of exogenous pathogens by forming a barrier.

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8
Q

Name the example given in lecture of an opportunistic pathogen.

A

Fusobacterium necrophorum

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9
Q

What is an opportunistic pathogen?

A

Normally does not cause disease in host, but if conditions change that favor growth of bacteria it can cause problems. (ie. ulcerations in stomach, alopecia in dogs, etc.)

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10
Q

What is pathogenicity?

A

It is the ability for the bacteria to cause damage in the host. Can the pathogen cause harm or not.

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11
Q

What is virulence?

A

The relative capacity of the pathogen to cause disease. How bad is the disease that is caused by the pathogen.

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12
Q

What is transmissibility?

A

How well the pathogen can spread from one host to a new host. Not whether or not the pathogen once in the host can cause an infection.

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13
Q

What size has the best transmission to the new host?

A

infectious droplet nuclei. this is why biological weapons are aerosolized.

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14
Q

How far can infectious droplet nuclei “fly”?

A

5 to 160+ feet

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15
Q

What is infectivity?

A

How well the pathogen, once in the new host, can settle down and cause disease. How well cell to cell spread of the bacterium occurs.

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16
Q

Describe what virulence factors are.

A

Traits that the microbe has that are able to cause pathogenicity. Basically what makes the bacteria/microbe dangerous to the host.

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17
Q

What are the common characteristics of genes that cause good virulence factors?

A

They are expressed as needed (faculatative)
They are distributed unevenly among strains of species
Can be spread via horizontal transfer
Cluster in pathogenicity islands

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18
Q

What do the virulence factors specifically aim to help the pathogen do?

A
Colonize host 
Evade host defenses 
Grow
Invade cells/tissues 
Cause damage
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19
Q

What are the three major categories of virulence factors?

A

Adhesins + Capsules + Toxins

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20
Q

What are adhesins?

A

Macromolecules that bind bacteria to host cells/tissues

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21
Q

Where are the adhesins located on the microbe?

A

Surface structures such as fimbriae, pili, glycocalyx

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22
Q

Describe in detail how the adhesins work.

A

Bind to receptors on target cells with high specificity causing a receptor-ligand interaction. This allows for the microbe to cause changes within the host cell.

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23
Q

What is important to know about the specificity of the adhesins? (What do they allow for)

A

Tissue tropism + Host specificity

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24
Q

What are E. Coli K88 infections limited to?

A

PIGS

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25
What is tissue tropism?
The microbe can only bind to a certain tissue. Things that are specific for the respiratory tract can't infect the GI tract (most of the time)
26
What is K88?
Adhesin on a strain of E. Coli that can only bind to certain receptors on the brush border of the pig enterocytes
27
What is one result, given in lecture, of the receptor-ligand interactionof adhesin to the host cell?
Causes the pathogen to be taken up by the host cell = increased chance of infection
28
What is the function of the capsule?
Impairs phagocytosis Mediates biofilm formation Prevents dessication
29
What is an example of a bacteria found on dental plaque?
Streptococcus mutans
30
What is used in a capsule stain?
India ink
31
What are two methods in which bacteria toxins cause damage to host?
At site of colonization/invasion | At sites remote from original point of invasion
32
What are the two major types of toxins that bacteria have?
Exotoxin + Endotoxin
33
What kind of bacteria tend to have exotoxins?
G+ and G-
34
What kind of bacteria tend to have endotoxin?
G-
35
When are endotoxins normally released?
Once cell is lyse, since these are found on the inside of the cell need the cell to "explode" in order for them to be exposed to the host.
36
What are the general effects of exotoxins?
Normally enzymes so they tend to have highly specific effects on the target cells and tissue they are involved with.
37
What general effects are normally caused by endotoxins?
Produced generalized, inflammatory related damage to the host. Hint: think of it this way. the body isn't exposed to these unless they are released. Therefore, immune response will be started.
38
What specifically on a gram-negative bacteria are considered endotoxins?
Lipid A which is present on LPS
39
What exactly does Lipid A cause in the body?
Stimulate leukocytes to release high levels of cytotoxin Activate compliment cascade Activate coagulation cascade
40
What are the side effects seen in the host from endotoxin release?
Fever + Chills + Weakness + Myaldia + Hypotension + DIC + Shock
41
What are the three components of LPS?
O-polysaccharide (O-antigen) Core polysaccharide Lipid A
42
What are the four major categories (effects) seen in exotoxins?
Enzymes that degrade the ECM Enzymes that act on plasma membrane Enzymes that act inside host cell Toxins that promote immune response = SUPERANTIGENS
43
What are the three components that make up an exotoxins name?
Host cell attacked Associated disease What microbe is responsible for the toxin
44
What is alpha-hemolysin?
Pore-forming toxin
45
What bacteria produces alpha-hemolysin?
Staphylococcus aureus
46
What medical importance do exotoxins have?
Inactivated forms can be used and turned into a toxoid that can be given as a vaccine.
47
What are the three basic steps in pathogenesis?
Colonization + Invasion + Damage
48
What are the portals of entry?
Mucous membrane Skin Direct deposition under the skin/membrane
49
What is it called when there is deposition under the skin or mucous membranes?
Paraenteral route
50
What are the two general methods that microbes can attach to host cells?
Non-specific + Specific
51
What is an example of non-specific adherence to host cells by microbes?
Capsules + bioflims
52
During colonization, what are three basic ways that microbes can evade the immune system?
Impair phagocytosis Evade complement Hydrolysis/break down of key immune components
53
What are ways that a microbe ensure nutrients to grow within their host?
Co-opt host nutrients + acquire nutrients via damage to host cells/tissues
54
What are siderophores?
Steal iron from iron-transport proteins in the host
55
What is an important characteristic of biofilms?
Facilitate quorum sensing + Allow development of high cell densities
56
What is quorum sensing?
Biofilm inhabitants are able to coordinate cellular activities
57
What is an important enzyme for invasion of the host by the microbe?
Invasins
58
What are three big examples of invasins used to invade the host?
Hyaluronidases Collagenases Elastases
59
What do invasins do?
Cause local damage to host cells + ECM
60
What are two methods that the microbes breach the epithelial barrier?
Paracellular + Transcellular
61
What are ways that pathogens spread in the body, organ to organ?
Peritoneal + Pleural cavities
62
What are the four basic ways that pathogens cause damage to the host?
Take up the host's nutrition Cause direct damage due to colonization/invasion Toxins Immune response due to presence of the pathogen
63
What is a subclinical infection?
Does not cause a noticeable illness within the host. Showing that infection does not always lead to disease.
64
What is an example given in lecture of subclinical infection?
Leptospira infections in dogs
65
What is an acute disease?
Quick to show signs and quick to end
66
What was an example of an acute disease given in the lecture?
Campylobacteriosis in dogs + cats
67
What is a chronic disease?
Tends to take a long time to show signs in the host. Can lay dormant for years. Can reactivate with stress or old age.
68
What was an example of chronic disease given in the lecture?
Tuberculosis in cattle
69
What are the portals of exit?
Normally pathogenic effects, commonly from the same route that it enters the body IE. coughing, sneezing, skin lesions. etc.
70
What are carriers? Why is it important to know about carriers?
These hosts show no signs or symptoms but are contagious and can pass the disease on to others. Dangerous because you could be exposed without even knowing it.
71
What is the pathogenesis of equine strangles?
Upper respiratory tract = nasal discharge
72
How is equine strangles transmitted?
direct or indirect transfer within nasal discharge
73
When does shedding of the bacteria responsible for equine strangles start?
1 to 2 days after onset of pyrexia, lasts for about 2-3 weeks
74
Describe mutualism.
Both the host and microbe benefit.