Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

BIO 315 > Module 12: Bacterial Pathogenesis (Overview + Attachment Proteins) > Flashcards

Module 12: Bacterial Pathogenesis (Overview + Attachment Proteins) Flashcards

(100 cards)

Start Studying
1
Q

Pathogenic Bacteria

A

Bacteria that survive in a living host by obtaining nutrients via tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Non-Pathogenic Bacteria

A

Bacteria that may live within a host but DO NOT cause tissue damage to obtain nutrients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the main difference between pathogenic and non-pathogenic bacteria?

A

Pathogenic = causes tissue damage

Non-pathogenic = does NOT cause tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diseases resulting from pathogenic bacterial infections are due to what? (2)

A

The pathogenic bacteria itself AND the immune response it triggers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pathogenesis

A

Process used by pathogens to produce disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 3 key requirement of bacterial pathogenesis?

A

1) Gain access to host tissue

2) Evade + overcome host defenses (once inside)

3) Obtain nutrients needed to multiply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do pathogenic bacteria typically acquire their needed nutrients?

A

By damaging their host’s tissues to obtain their nutrients OR by stealing the nutrients away from their host/s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is key to pathogen evolution?

A

Genetic mobility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Virulence Factor

A

(VF) A product made by a pathogen that enhances its ability to cause disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

VFs are very diverse BUT they are similar in what way?

A

They act in common ways

Specifically act to carry out the 3 key requirements of pathogenesis (access host tissue, evade immune response, obtain nutrients)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the main VFs of Neisseria gonorrhea?

A

1) Fimbriae

2) LOS (endotoxin)

3) IgA Protease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the function of fimbriae in N. gonorrhea?

A

Allows N. gonorrhea to attach to the epithelial cells of the cervix and/or urethra and subsequently allowing for invasion of underlying tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the function of LOS N. gonorrhea?

A

LOS = Lipooligosaccharide (Endotoxin)

Evokes an intense inflammatory response in host causing tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does tissue damage caused by LOS lead to in What is the function of fimbriae in N. gonorrhea?

A

1) Facilitates the invasion of N. gonorrhea leading to the acquisition of nutrients

2) Causes symptoms of gonorrhea disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes tissue damage in N. gonorrhea

A

2 components:

1) LOS induced inflammatory response

2) Other enzymes produced by N. gonorrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the function of IgA Protease in N. gonorrhea?

A

IgA protease degrades host IgA antibodies (Abs) leading to immune evasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does N. gonorrhea evade host immune response?

A

2 main ways:

1) Via IgA protease degradation of host IgA antibodies

2) By continuously changing its surface antigens (mainly the fimbriae structure) == renders host antibodies ineffective!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Overall, how do the 3 VFs produced by N. gonorrhea relate to the 3 key requirements of bacterial pathogenesis?

A

Fimbriae = For attachment; allows access to the host tissue

LOS (endotoxin) = Causes tissue damage; allows for nutrient acquisition

IgA Protease = Immune response evasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why is attachment important for pathogenic bacteria?

A

Without proper attachment most bacteria would be removed by friction, fluids ,or displaced by other microbes

(Decreasing infection)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Non pathogenic bacteria do NOT usually _____________ instead they ______________

A

Non pathogenic bacteria do NOT usually attach directly to host cells instead they colonize extracellular surfaces of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Attachment Factors

A

VFs used by pathogens to attach to host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the most commonly utilized types of attachemnt factors?

A

1) Fimbriae
2) Fibronectin-Binding Proteins
3) Membrane Associated Molecules
4) Specialized Attachment Proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is fibronectin?

A

A large glycoprotein that is found extensively throughout the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where is fibronectin found in the body?

A

1) Circulating in blood plasma

2) As fibers in the extracellular matrix (ECM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is fibronectin's role as an ECM fiber?
Anchors cells to support surfaces (like basement membranes or collagen)
26
Fibronectin binding proteins are most well studied in what strains? (Are they (+) or (-) gram?)
E. coli (-) Staphylococcus aureus (S. aureus) (+) Streptococcus pyogenes (S. pyogenes) (+)
27
What is the role of fibronectin BPs in *S.aureus*?
Once S. aureus gets into the blood stream --> Fibronectin BPs allow for attachment and invasion of vessel walls --> Pathogenic bacteria allowed to move into surrounding tissues --> S. aureus makes it to heart and colonizes the heart valves (CAN, not definite) == Endocarditis
28
Fibronectin BPs are predominant adherance factors for what surfaces?
1) Skin 2) Nasal mucosa 3) Endothelial lining of RBCs
29
Fimbriae
= Specialized pilli primarily used for attachment
30
What is the critical structural element of fimbriae?
The END of each fimbria strand which has an ADHESIVE TIP (made of a tip protein) --> Is what allows for fimbria attachment to host cells!
31
Why are fimbria tip proteins needed?
Fimbria tip proteins bind to the receptors on host cells == allows for attachment!
32
Fimbria can adhere to what kinds of surfaces?
Biological (Ex: tissues) and NON-biological surfaces (Ex: medical implants)
33
How does fimbria assembly occur?
Occurs in a sequential manner bottom --> up --> The fimbria strand grows from its base through the addition of pillin subunits that "push" the tip protein up and away from the cell surface
34
What main advantages do fimbriae provide? (2)
1) Allows for attachment even with cell-cell repulsion (overcomes electrostatic repulsion) 2) Immune system evasion
35
What is the issue of electrostatic repulsion between cells? Why is this a problem for pathogenic bacteria?
The surface molecules of cells generate an overall net NEGATIVE charge on the surface of cells! == Cells repulse each other due to the like charges --> A problem for pathogenic bacteria because it prevents their attachment (since the bacterial cell can't get close to host cell without being repulsed away from it)
36
What bacterial "solution" is employed to mitigate attachment issues due to cell-cell repulsion? HOW?
Fimbriae! --> Fimbriae allow bacterial cells to attach to host cells without getting so close to them! == **Fimbriae SPAN the distance of the repulsion, attaching the cells while keeping them positionally separated!
37
How do fimbriae aid with immune system evasion?
Fimbriae are very dynamic! --> Constantly changing nature makes it hard for the immune system to target these VFs!
38
What types of variation do fimbriae present/undergo that aids in immune system evasion?
1) Antigenic Variation 2) Phase Variation
39
Antigenic Variation: What does it mean for fimbriae? (How does it help immune evasion?)
**The changing of AA sequences of expressed fimbriae proteins via genetic recombination!** == Constantly changing "antigen" (the fimbriae) = host-developed antibodies only work for short period of time before becoming ineffective (due to the changing antigen!)
40
How are antigenic and phase variation generated?
Via genetic recombination between different fimbria genes and genes/signalling molecules in the environment!
41
Phase Variation: What does it mean for fimbriae?
The "turning on or off" of fimbriae expression! (Change in the presence or absence of fimbriae altogether or for specific TYPES)
42
How does phase variation of fimbriae aid in host immune evasion?
The changing expression of different fimbriae makes it difficult for the immune system to generate an effective response as the fimbriae they generate a response against change, rendering the generated response ineffective
43
What is an example of a bacteria that use fimbriae for their pathogenesis (other than N. gonorrhea)?
Uropathogenic E. Coli == Causing UTIs
44
The constant **appearance/disappearance** and protein sequence changes in fimbriae makes them a __________ to the ___________ immune system
The constant appearance/disappearance and protein sequence changes in fimbriae makes them a **"MOVING TARGET"** to the **ADAPTIVE** immune system
45
What VFs do N. gonorrhea use to adhere to their host cells? (What are their host cells?)
N. gonorrhea uses FIMBRIAE to attach to epithelial cells of the cervix and urethra
46
What membrane associated molecules act as attachment factors in GRAM (+) bacteria?
Gram (+) = **Outer membrane proteins**
47
What membrane associated molecules act as attachment factors in GRAM(-) bacteria?
Gram (-) = **Lipoteichoic Acids** (LTAs)
48
What is an example of specialized attachment proteins that act as attachment factors? (What biological system?)
The **Tir + Intimin** system within **Enteropathogenic E. coli** strains!
49
Enteropathogenic
Causing disease within the intestinal tract
50
What are enterocytes?
Epithelial cells lining the intestinal mucosal surface (basically the cells of the intestine doing the absorbing)
51
What cells do enteropathogenic E.coli infect?
Enterocytes
52
Enteropathogenic E. coli attach to enterocytes using what mechanisms?
TWO mechanisms! 1) Fimbriae binding to glycoproteins 2) Specialized attachment protein system: Tir + Intimin
53
What are Tir + Intimin?
BOTH are proteins made by enteropathogenic E.coli **Tir**= Translocated Intimin Receptor; a receptor located on HOST cell (enterocyte) surface that binds to the E.coli VF, intimin **Intimin** = A surface protein of enteropathogenic E. coli (VF)
54
How does Tir come to be presented on enterocytes? Explain the steps:
Through a Type III secretion system from enteropathogenic E. coli 1) E. coli strain synthesizes Tir in its cells 2) Tir is translocated to the host cell (enterocyte) via a Type III Secretion System (direct injection via channel) 3) Once inside the host cell, Tir gets expressed on the surface of the host cell microvilli
55
What happens when E.coli intimin binds to the Tir presented on host cell microvilli?
A pedastal (lesion) forms! == The binding event triggers a disruption in cell signaling pathways that leads to the induction of cytoskeleton changes, primarily the polymerization of Actin (near the binding site!) == Loss of microvilli and formation of a pedastal!
56
What is the entire process of enteropathogenic E. coli attachment to host cells ? (AND how it leads to pathogenesis)
1) enteropath. E. coli synthesizes Tir + Intimin 2) Tir is translocated to host cell via an E.coli Type III Secretion System 3) Tir is presented on the surface of host cell + intimin is presented on surface of E.coli 4) Tir + intimin BIND 5) Binding event triggers cytoskeltal changes (polymerization of actin) 6) Cytoskeletal changes cause the deformation of microvilli, producing a pedastal == loss of enterocyte function!
57
How does pedastal formation differentially impact enteropathogenic E.coli and enterocytes (+ the host)?
**E. coli = BENEFITS them**; Projects these pathogens further into the lumen, allowing for less competition with other microbes and greater access to nutrients! **Enterocytes/Host = BAD for them**; loss of microvilli decreases nutrient absorption and increases tissue degeneration!
58
What is a lesion?
A change or abnormality in a cell or tissue
59
What is a pedastal AKA?
Attachment + Effacing Lesion (AE Lesion)
60
Capsule
A loosely organized matrix of polymers surrounding some bacterial cells
61
What polymers can capsules be made of?
Most commonly made of polysaccharides BUT can be made of polypeptides as well
62
What is a capsule AKA?
Glycocalyx
63
What is the main role of a capsule in pathogenicity?
EARLY- Immune system evasion! --> Protecting against phagocytosis and lysis by complement
64
What are the two main immune responses that capsules protect pathogenic bacteria from?
1) Phagocytosis 2) Lysis by complement (opsonization)
65
Opsonization
A method of tagging pathogens for elimination by immune cells --> Tags = opsonins
66
Opsonins
Molecular tags that bind to non-self materials allowing for their targeted destruction == Antibodies OR complement proteins
67
Opsonization/phagocytosis process for NON-encapsulated pathogen:
1) Free floating opsonins such as Abs + cb3 bind to the pathogen's host surface 2) Bound opsonins are recognized by phagocyte receptors 3) The phagocyte binds to the pathogen via its bound opsonins 4) Binding triggers phagocytosis to occur 5) Endocytic pathway can commence = presentation of pathogenic antigens by macrophages for T-cell activation
68
Opsonization/phagocytosis process for encapsulated pathogen:
1) Free floating opsonins such as Abs + cb3 DIFFUSE through the capsule and bind to the pathogen's cell surface 2) Bound opsonins are buried within the capsule == phagocytes receptors can't interact with them 3) No phagocytic recognition = no phagocyte binding = no phagocytosis AND no entry into endocytic pathway == IMMUNE EVASION!
69
cb3
A complement protein (opsonin)
70
What are the receptors for cb3 and Abs?
cb3 receptor = phagocyte CR3 ABs Receptor = FcR --> Antibodies bind to FcR via their Fc region! (base of the Y structure!)
71
How do capsules prevent phagocytosis?
By rendering opsonins ineffective --> Blocking opsonin-phagocyte receptor interaction!
72
A decrease in phagocytosis causes a decrease in what other immune response?
Decrease Antibody targeted response! (T-cell activation; adaptive immune system)
73
How can host cells "get around" the issue of opsonin blocking via the presence of a capsule?
By using Anti-capsule antibodies! == Abs that bind to the CAPSULE ITSELF! == Allows for phagocytes to bind and destroy encapsulated pathogens
74
Some bacteria produce capsules made of what material for immune evasion?
Capsules made of "self" molecules!
75
What are the benefits of "self" capsules?
It discourages opsonization (a process that usually only occurs in response to FOREIGN materials) == prevents stimulation of the antibody/complement response! = no immune response! (Pathogen is disguising itself as the host!)
76
Serum Resistance
Prevention of complement factor deposition on pathogen when in serum containing free complement factors
77
Avoiding some or all of the EARLY immune defenses of a host allows a pathogen to...
Replicate to high enough numbers to outpace the host immune defenses
78
OTHER than immune evasion, what protective roles do capsules play?
1) Prevent phage infection! 2) Prevent dessication! (capsules contain water for this reason!)
79
What is the capsule of Bacillus anthracis made of?
Poly-D-glutamic acid (B. anthracis causes anthrax)
80
What is the capsule of Streptococcus pyogenes made of?
Hyaluronic Acid
81
What is the capsule of Haemophilus influenzae made of?
6 different capsule types
82
What is the capsule of Neisseria meningitis made of?
Sialic Acid
83
What is the capsule of Pseudomonas aeruginosa made of?
Alginate (biofilm formation)
84
What are the 3 ways in which pathogenic bacteria release toxins or VFs?
1) Cell lysis 2) Secretion to the external environment 3) Injecting directly into host cell
85
What class of bacteria use Type III + IV secretion systems?
Gram (-)
86
What do Gram (+) bacteria use instead of secretion systems?
Cytolysins --> They lyse cells to release toxins or VFs
87
Type III Secretion System
An injection assembly that delivers VFs DIRECTLY into the host cell by forming a channel
88
What layers does the Type III Secretion System channel go through?
The channel goes through: 1) Bacterial PM 2) Bacterial OM 3) Host PM
89
Of the two "injection systems", which one is more common
Type III !
90
Type IV Secretion System
A system that delivers molecules across PMs to "inject" VFs via a "conjugation-like" mechanism
91
What is the main difference between Type III + IV secretion systems?
The structure they form/use to transfer materials Type III = "Needle-like" structure for injection Type IV = Pilus-like structure
92
What is a key limiting nutrient for pathogens? WHY?
IRON --> Because iron is kept TIGHTLY BOUND by host iron binding proteins! (= very little free iron to obtain)
93
List the main methods employed by pathogenic bacteria to acquire iron from hosts?
1) Siderophores 2) Transport Proteins 3) Acidic (Low pH) Metabolites 4) Cytolysins
94
Siderophores
Bacterial iron-binding proteins that bind iron from surrounding medium
95
Within a host, siderophores can...
Obtain iron in TWO ways! 1) COMPETE with host iron-BPs for FREE (unbound) iron in solution 2) STEAL already-bound iron from host iron-BPs!
96
How do siderophores STEAL iron from host iron-BPs?
Siderophores that have a very high binding affinity for iron may be strong enough to TAKE the BOUND iron from the host iron-BP
97
How do pathogenic bacteria use transport proteins to acquire iron?
The transport proteins produced by pathogenic bacteria can bind to the host-ironBPs themselves (those CARRYING iron) and bring the entire iron bound-host iron BP complex to the bacterial cell ==> Lets the host do the iron binding FOR the bacteria!
98
How do acidic metabolites aid in iron acquisition?
Pathogenic bacteria can produce acidic/low pH metabolites to lower the pH of the region near the site of infection --> This low pH/acidification causes changes in the host iron-BP structure that leads them to RELEASE their iron (cannot keep the iron bound) == Makes iron available for the bacteria to take!
99
How do pathogenic bacteria use cytolysins to aid in iron acquisition?
SOME bacteria produce cytolysins (like hemolysins = lyse RBCs) that lyse host cells to release their iron stores and other nutrients
100
Cytolysins allow bacteria to gain access to...
INTRACELLULAR iron stores + nutrients!

BIO 315 (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions