Adhesion and Invasion Flashcards

(77 cards)

1
Q

What is adherence essential for both extracellular and intracellular bacteria?

A

Extracellular: adherence allows bacteria to resist the mechanical clearing mechanisms of the host
Intracellular: pre-requisite for uptake or invasion

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2
Q

What are adhesions?

A

Bacterial components that mediate interaction between the bacterium and the host cell surface

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3
Q

How do adhesions bind to host cells?

A

They bind specifically to host cell surface receptors
There is a high degree of specificity between adhesion and the host recognition site

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4
Q

What are host surface glycans used for?

A

Receptors for bacterial adhesions as bacteria can specifically recognize and adhere to sugars

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5
Q

What are pili?

A

Fragile, hairlike adhesions that are frequently replaced and thus have a high potential for variation

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6
Q

How do pili hide their antigenic site?

A

The are highly glycosylated which allows for velcro-like attachment to surfaces

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7
Q

What are Type 1 pili and what Gram stain are they found on?

A

Rigid, long (0.5-10 micrograms), and thin filaments that protrude off Gram-negative bacteria

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8
Q

What is a unique feature of type 1 pili?

A

They induce hemagglutination

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9
Q

How are type 1 pili assembled and by which pathways?

A

Composed of polymerized subunits of the pilin protein = sec-transport pathway
Chaperone-usher pathway assembles proteinaceous filaments of bacterial surfaces

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10
Q

What do type 1 pili operons, at minimum, encode?

A

Chaperones, usher, and pilin

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11
Q

What are F1 pili?

A

Short, linear, and flexible polymers that have a tendency to aggregate

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12
Q

What are F1 capsular antigens exclusively expressed by and what is its function?

A

Y. pestis
Anti-phagocytic which prevents uptake by macrophages

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13
Q

What is a similarity between F1 pili and type 1 pili?

A

They both use the CU system

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14
Q

What does the F1 capsule consist of and what is its characteristic?

A

A tangle of thin, linear Caf1 fibers
Lots of variabilities = limited vaccine development

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15
Q

What are 3 examples of bacteria with type IV pili?

A

EPEC
N. gonorrhoeae
N. meningitidis

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16
Q

What does the binding of EPEC cause?

A

Upregulation of virulence genes in bacterium and retraction of the pilus

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17
Q

What do type IV fibers recognize?

A

Host cell sugars

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18
Q

What can EPEC and V. cholerae type IV pili do?

A

Aggregate laterally forming bundles

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19
Q

How does twitching motility work?

A

Surface motility powered by the extension and retraction of type IV pili, which confers slow cell movement that appears jerky

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20
Q

What is motility required for in type IV pili?

A

Required for virulence and may help engage the type II secretion systems for the injection of toxins

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21
Q

What is microbial dysbiosis on the teeth facilitated by?

A

A shift in the microbiome towards Gram-negative anaerobes

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22
Q

What is the keystone pathogen causing periodontal disease and is this pathogen alone sufficient to cause the disease?

A

P. gingivalis
It is not sufficient on its own but instead facilitates an ecological change to a disease state

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23
Q

How dos P. gingivalis act as a keystone pathogen?

A

By the production of a virulence factor called gingipain (cysteine protease)

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24
Q

How does gingipain work?

A

It cleaves complement C5 protein into C5a which activates the C5a receptor and increase the inflammatory response but at the same time prevents microbial killing by leukocytes

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25
Which pili are the only ones that can bind DNA?
Type IV
26
What does DNA transformation from N. meningitidis require the presence of?
Short DNA uptake sequences residing in coding regions of the donor DNA
27
What does transferred DNA often contain?
Virulence genes including toxin resistance and antibiotic resistance
28
Where do meningococcal type IV pili bind DNA?
Through the minor pilin ComP which is a highly conserved component throughout Neisseria species
29
What do type IV pili promote?
The attachment to a variety of chemically diverse surfaces
30
What are biofilms?
Dense, multi organismal layers of bacterial communities attached to surfaces
31
What is the attachment of biofilms to surfaces mediated by?
Extracellular polysaccharide slime (EPS)
32
What are the primary colonizers of biofilms?
Clostridia spp and P. aeruginosa
33
What is P. aeruginosa and what does it cause?
A typically nosocomial, opportunistic pathogen It causes UTIs, respiratory infections, and GI infections
34
What is the natural habitat of P. aeruginosa?
Ubiquitous in soil and water
35
What is the metabolism of P. aeruginosa like?
Metabolically diverse, can be aerobic or anaerobic Can grow on 75 different organic substrates
36
What are the nutritional requirements of P. aeruginosa?
Minimal nutritional needs
37
What is the optimal growth temperature of P. aeruginosa?
Wide temperature range, 0-37 degrees
38
What is the tolerance of P. aeruginosa to physical conditions like?
Often grows in biofilms Resistant to detergents and high salt
39
How is P. aeruginosa resistant to antibiotics and phagocytes?
Antibiotic-resistant genes have evolved Association with biofilm
40
What does P. aeruginosa produce to adhere to the host or other surfaces?
Type IV pili
41
What is the process of biofilm formation?
Type IV pili produce EPS Association with type IV pili with a substrate activates PSl genes which are involved in the formation of the biofilm The early stages of biofilm formation have low levels of EPS and is reversible at this point The accumulation of EPS causes a thick biofilm that allows for immune invasion and resistance to insults
42
What are PSl genes?
Polysaccharide synthesis locus genes
43
What do sortase enzymes do?
Catalyze the transpeptidation of pilin synthesis, linking of amino acids
44
What is an important virulence factor for Gram-positive bacteria?
Sortase enzymes
45
How are Gram-positive pili formed?
By covalent attachment of pilin subunits to each other and to the peptidoglycan layer
46
What do prokaryotic sortase enzymes promote?
The covalent anchoring of surface proteins to the cell wall envelope to enable each microbe to effectively interact with its environment
47
What are the main functions of sortases?
Cleave surface proteins and allow rearrangements and modifications Sorts proteins of the cell surface and covalently links to the cell wall Polyermizes pilin proteins
48
What are the symptoms of diphtheria?
Sore throat Grey patches in the throat Barking cough
49
How many sortase enzymes does C. diphtheriae encode and how many does it actually need?
Encodes 6, only needs one
50
What is the purpose of SpaA?
Produces shaft of the pilus (type III)
51
What is SrtA?
The sortase that polymerizes pilus
52
What is SpaB?
Surface proteins
53
What is SpaC for?
Tip adhesion
54
What is the purpose of SrtF?
Housekeeping sortase that anchors pili into the cell wall
55
What system exports pilin proteins?
Sec transport system
56
How does S. aureus disguise itself?
Sortases function to attach immunoglobulins to the surface of the bacteria
57
Can mutants of SpaA cause infection?
No
58
What do non-pili adhesins facilitate?
Tighter binding of bacteria to host cells after initial binding by pili
59
What type of bacteria are non-pili adhesions common in?
Gram-positive food-borne pathogens
60
What is YadA and what does it promote?
A collagen-binding outer membrane protein that promotes cell adhesion to eukaryotic host and virulence
61
How does YadA protect bacteria?
Binding ECM Temperature sensitive expression Pro-phagocytic
62
Which bacteria is YadA found in?
Y. pestis Y. pseudotuberculosis Y. enterocolitica
63
What are 3 virulence factors of Yersinia?
LPS YadA Invasin
64
What is the difference between YadA and invasin?
YadA interacts indirectly with integrins though binding of the ECM Invasin interacts directly with integrins
65
What do YadA and invasin trigger?
Entry into phagocytes as invasin zippers host membrane around it
66
What do many pathogens do once adhered?
Use the cell's own cytoskeleton to invade the target cell either by triggering phagocytosis or by using the cytoskeleton to migrate through the cell
67
What are the main adhesins and receptors in Listeria?
Adhesions = internalin A (InlA) and internalin B (INlB) Receptors = E-cadherin and Met
68
What are E-cadherin and Met components of?
Eukaryotic intracellular junctions
69
What exactly are InlA and InlB and what do they do?
Afimbrial adhesins Necessary and sufficient to trigger host cell entry
70
What does the entry of L. monocytogenes into cells require?
Requires action polymerization and membrane remodeling
71
What does L. monocytogenes manipulate to its advantage?
Host-cell signaling and endocytic pathways
72
What do actin rearrangements due to the binding of listeria form?
Pseudopodia
73
What does listeria binding to the host cause and what does it facilitate?
Microfilament rearrangement and it facilitates phagocytosis
74
Where does listeria thrive?
In phagosomes
75
What does InlA induce?
Cytoskeletal rearrangements in the host cell for uptake of listeria by epithelial cells = virulence factor
76
What is E-cadherin and what binds to its extracellular domain?
Host protein Transmembrane, cell-cell adhesion molecule InlA binds to the extracellular domain
77
Assembly and attachment of what is central to intercellular adhesion and Listeria entry?
E-cadherin, alpha-catenin, beta-catenin