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MICR 341 - Quiz 4 > module 4.1 > Flashcards

module 4.1 Flashcards

1
Q

What are the three generalized steps of successful bacterial infection?

A

1) Colonization
2) Spread
3) Persistence

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2
Q

at what general step does the population of bacterial cells increase exponentially?

A

colonization

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3
Q

what is an accidental pathogen and what is an example of one?

A

An accidental pathogen is a pathogen that does not mean to enter the body but does.
Example: Legionella

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4
Q

what kind of pathogen is an STD?

A

intracellular obligates - STDs only stay between humans

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5
Q

what other reasons, besides to infect, are virulence factors used for mainly?

A

To survive the extracellular environment

e.g., other bacteria, antibiotics, UV light, etc.

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6
Q

bacterial pathogens are bacteria specialized for …

A

evading the immune system

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7
Q

what are the 4 major problems bacteria face in the environment?

A

1) Sequestration of iron
2) Adhesion sites
3) Exposure to noxious chemicals
4) exposure to sunlight and extreme weather

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8
Q

what kind of pathogens contain larger genomes, and why?

A

nonobligate, host-associated, and free-living microorganisms contain larger genomes than an intracellular obligate pathogen would because they need more tools to be able to survive freely in the environment
e.g., more fimbriae

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9
Q

what is the importance of endospores?

A

endospores protect bacteria against deleterious situations/ conditions, i.e., preserve bacteria’s genetic material from any external environmental factor

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10
Q

what bacteria are known for producing endospores?

A

1) bacillus

2) clostridium

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11
Q

what other mechanisms besides the formation of endospores, do bacterial pathogens have to protect against external damage?

A

DNA repair, efflux pumps, change in membrane properties, and detoxification

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12
Q

What are biofilms?

A

extracellular matrices/ gooey layers produced by bacteria that have colonized a surface. contains carbohydrates, proteins, and maybe even DNA that would form filaments to hold everything together

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13
Q

biofilms are a constant source of …

A

PAMPs- causes constant activation of the immune system

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14
Q

what is the level of resistance of biofilms?

A

very much resistant - resistant to antibiotics, disinfectants, and predators for the most part

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15
Q

what bacterial pathogens are able to cause the formation of biofilms in humans?

A
  1. pseudomonas aeruginosa

2. staphylococcus viridans

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16
Q

what infection is pseudomonas aeruginosa responsible for?

A

cystic fibrosis - formation of biofilms on lungs

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17
Q

what is the significance of staphylococcus viridans?

A

commensal bacteria, form biofilms/plaque on teeth

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18
Q

what is the main way biofilms are transmitted?

A

transmitted from medical devices such as a catheter. if too much biofilm enters the bloodstream it will cause septic shock

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19
Q

what is the significance of flagella?

A

produced by bacteria to swim through liquids and travel through viscous medium

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20
Q

what virulence factor contributes to the production of flagella

A

motility- critical for bacterial pathogens to reach their preferred site of infection

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21
Q

what receptors in the host are flagellins recognized by?

A

TLR5 and NOD-like receptors - PAMPS

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22
Q

Flagellins are highly …

A

antigenic

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23
Q

because flagellins are highly antigenic, what do bacterial pathogens do in order for successful infection?

A

tightly regulate the production of flagellins, stopping production once they are inside the host
e.g., phase variation used by Salmonella to trick the immune system

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24
Q

how do Treponema pallidum and Borrelia burgdorferi regulate their flagellin?

A

flagellum stays in the periplasmic space once inside the host

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25
Q

what infection is Treponema pallidum responsible for?

A

syphilis

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26
Q

what disease does Borrelia Burgdorfer cause?

A

lyme disease

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27
Q

how do flagellum move in Treponema pallidum?

A

moves in a screw-like motion - to penetrate the host membrane

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28
Q

bacteria use … as ways to penetrate the skin

A

vectors

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29
Q

what are examples of bacteria that use vectors to penetrate intact skin?

A
  1. Yersinia pestis, bypasses the skin layer and enters the bloodstream by a flea bite
  2. Borrelia Burgdorfer - uses ticks to cross the skin barrier, causing lyme disease
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30
Q

where does Yersinia pestis come from?

A

rodents

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31
Q

how is yersinia pestis transmitted from rodents to humans?

A

infected rodent transmits the bacterial pathogen to an insect that bites the rodent. The infected insect (flea vector) then bites humans causing outbreaks

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32
Q

what is the main cause of yersinia outbreaks?

A

living in densely populated areas that have a lot of rodents running around

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33
Q

why was it so easy for scientists to recover the whole genome of yersinia pestis and study its evolution?

A

there were huge outbreaks which gave scientists a large source of infected individuals to put together a genome. yersinia pestis outbreaks also occured for a very long time so scientists were also able to study the genomic changes from infected individuals from different periods of time

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34
Q

Lyme disease transmission

A

transmission runs through deer and rodents which ticks feed on. these infected ticks are then able to survive for a while in the environment. they then latch on to pets and humans transmitting Lyme disease.

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35
Q

what virulence factor in bacteria allows for sufficient attachment to host cells?

A

production of adhesins

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36
Q

what are adhesins?

A

protein structures that recognize a molecule of the host and bind to it

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37
Q

what are the two categories of adhesins?

A
  1. pili

2. afimbrial adhesins

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38
Q

what kind of response does the attachment of the pathogen to the host cell trigger?

A

a transcriptional response

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39
Q

what types of pili exist?

A
  1. thin filament
  2. curly pili, aggregation
  3. type IV pili, rope-like
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40
Q

what is the structure of gram-negative pili?

A

rod-shaped filamentous protein structures. a whole variety differing in thickness and length

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41
Q

what are the protein-subunits of pili?

A

pilin. polymerization of these protein subunits forms pili.

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42
Q

how are pilin subunits packed?

A

packed in an ordered fashion, into a helical array to form a flexible cylindrical structure

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43
Q

what section of the pilus is the actual adhesin?

A

the tip. recognizes and attaches to a molecule on the surface of host cells

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44
Q

definition of tropism?

A

the specificity an adhesin of a particular species of bacteria, has for a particular host protein. contributes to host cell- or tissue-specific interaction. only the body sites expressing the specific molecules will be infected

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45
Q

what are typical targets of adhesins?

A

carbohydrate residues (sialic acid), glycoproteins, and glycolipids

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46
Q

what system assembles most pili?

A

the chaperone-usher system

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47
Q

how does the chaperone-usher system work?

A

consists of protein synthesis in the cytoplasm, proteins are secreted into the periplasm where they’re ushered via chaperones along with other synthesized proteins, assembling the pili. the adhesive tip structure is assembled first, then the shaft of the structure and then a termination protein that stops the polymerization process.

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48
Q

what are the properties of pili of gram-negative bacteria?

A

bacteria constantly lose and re-form pili. they can be easily broken off by mechanical shearing.

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49
Q

why is losing and re-forming pili for bacteria beneficial?

A

if host antibodies are bound to the adhesin of the pilus, which blocks binding to host cells, and that pilus is then lost, the antibody will also de-attach from the bacterial cell membrane and form a new pilus with no antibiotic on it. increases the bacteria’s chance of evading the immune system.

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50
Q

why do gram-negative pili help bind to host cells?

A

if the host membrane is also negatively charged, the pilus is able to overcome the electrostatic repulsion present between the gram-negative bacteria and the host cell. the pilus does this by mediating loose binding to host cells, keeping the bacteria and host cell initially at a distance. when surface adhesins are produces, they will then mediate closer attachment

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51
Q

What is Type IV pili?

A

a special type of fimbriae that is not made via the chaperone-usher system. It is made in the inner membrane and the shaft component protrudes through the periplasm and the outer membrane.

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52
Q

what is the significance of type IV pili’s shaft?

A

can extend (polymerize) and de-extend (depolymerize). once attached to a host cell, the shaft will depolymerize, bringing the host cell closer to the bacteria, using the PilA component.

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53
Q

what are the characteristics of pili in gram-positive bacteria?

A

short and thin

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54
Q

what kind of molecular bond is formed between gram-positive pili?

A

covalent bond

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55
Q

covalent attachment of gram-positive pili to the peptidoglycan layer occurs via …

A

sortase - a protein only in gram-positive bacteria

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56
Q

what motif mediates the attachment of pilin subunits to the peptidoglycan cell wall

A

LPXTG motif

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57
Q

what are nonfimbrial adhesins?

A

bacterial surface proteins that mediate attachment to the host cell surface

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58
Q

what type of ligands on host-cell surfaces mediate attachment of host cells to surrounding tissues?

A

integrins and cadherins - interact with the extracellular matrix

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59
Q

what two surface proteins do listeria monocytogenes use to bind to host cells?

A

internalin A and internalin B

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60
Q

yersinia pestis invasin binds to …

A

alpha5beta1-integrin

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61
Q

invasin alpha5beta1-integrin shares structural features with …

A

fibronectin, the natural host ligand of alpha5beta1-integrin

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62
Q

what does internal A bind to? (Listeria)

A

E-cadherin (tight junction)

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63
Q

what does internalin B bind to?

A

the receptor for the subunit C1q (receptor gC1qR) of the complement protein C1 , located on the host cell surface

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64
Q

… is one of the least understood virulence factors?

A

penetrating and moving through the mucin layer to reach the underlying epithelial cell layer

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65
Q

the layer of mucin is not a …

A

uniform mat - bacteria that can produce enzymes to degrade the mucin layer still consists of a long process because of the complexity of the mucin layer

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66
Q

mucin is secreted by __ cells

A

goblet cells

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67
Q

what cells can bacteria travel through, overtaking the mucin layer?

A

M cells - not covered by a thick mucin layer because they are not closely located to goblet cells

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68
Q

what is the significance of H. pylori regarding the mucin layer?

A

able to penetrate through the mucin layer, by increasing the mucin’s pH . the increase in pH causes the mucin to de-gel, allowing the bacteria to travel through and reach the gastric epithelium

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69
Q

what enzyme do H. pylori use to raise the mucin’s pH?

A

urease - converts urea to ammonia, neutralizing the gastric acid

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70
Q

inflammation due to H.pylori invasion is due to ___ components

A

gastric acid, proteases, and effector molecules released by H. pylori

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71
Q

what is the significance of the production of ammonia produced via urease by H. pylori?

A

neutralizes the gastric acid and results in mucosal cell death along with production of cytokines due to inflammation

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72
Q

what is the mechanism role of sIgA?

A

simultaneously binds to the bacterial antigen via their antigen-binding sites and interact with mucin via their Fc portion - effectively traps bacteria in the mucin layer

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73
Q

what is bacterial mechanism against sIgA?

A

production of an sIgA protease - cleaves sIgA at the hinge region which separates the part of sIgA that binds to mucin from the part that binds to the antigen

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74
Q

the mucus layer contains ___ secreted by underlying host cells.

A

Antimicrobial peptides (AMP)

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75
Q

4 mechanisms of resistance to AMP by bacteria:

A
  1. capsule (isolation from AMP)
  2. LPS or LTA/TA modification (addition of a positive charge)
  3. peptidases
  4. efflux pumps
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76
Q

once pathogenic bacteria evade the immune system, they can __

A

grow and acquire nutrients

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77
Q

how do some bacteria avoid the recruitment of phagocytes?

A

produce enzymes that degrade C5a

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78
Q

what source of PAMPs can bacteria modify to be less recognized by the host immune system?

A

LPS - causes a reduction of the host response

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79
Q

some bacteria produce ___ that kill phagocytes, prevent their activation, inhibit their migration, or reduce the strength of the oxidative burst

A

toxins

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80
Q

what toxin do H. pylori produce?

A

VacA

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81
Q

what different roles can VacA perform?

A

effects on cell signaling, pore formation in the cell membrane, vacuolation, apoptosis, etc.

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82
Q

what is the significance of capsules?

A

forms a protective coating around bacteria - an unstructured network of polymer

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83
Q

what immune system components does the capsule protect bacteria from?

A

lysosomes, antimicrobial peptides, phagocytosis (opsonization and digestion), and the complement system

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84
Q

how does the capsule protect against the complement system?

A

capsules have a low binding affinity for the B factor or have a preference for the H factor (B factor located on complement proteins, i.e., C3b, C5b)

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85
Q

what is an effective host response against encapsulated bacterial pathogens?

A

producing antibodies that bind to the capsule and promote phagocytosis and activation of the complement by the classical pathway

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86
Q

capsules that resemble ___ are poorly immunogenic

A

host polysaccharides

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87
Q

___ serve as a site of attachment for C3b

A

LPS

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88
Q

what do bacteria attach sialic acid to, in order to inactivate C3b (H/I factor)

A

LPS O antigen

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89
Q

what is the significance of bacteria expressing long O antigens?

A

to cause the MAC complex to form far away from the bacterial membrane and render it ineffective

90
Q

what mechanism allows for evading the host’s antibody response?

A

antigenic variation, capsule resembling host polysaccharide, and coating of bacteria with host proteins

91
Q

definition of intracellular pathogens

A

bacteria that live inside the host cells

92
Q

some bacteria have evolved ways to invade non-phagocytic cells by inducing ___ reorganization by using ___ or ___

A

actin

invasins or T3SS

93
Q

example of non-phagocytic cells

A

mucosal cells

epithelial cells

94
Q

what occurs inside the host cell when Listeria’s internalin A (InlA) component binds to E-cadherin and its InlB component binds to gClqR?

A

actin cytoskeleton rearrangements and signaling

95
Q

why are bacteria like Yersinia and Mycobacterium considered such dangerous bacterial pathogens?

A

they are able to overcome the phagocyte’s strategies to kill bacteria

96
Q

what is the host cell response to pathogens who are trying to overcome phagocytosis?

A

activation of the macrophage response (mediated by T-helper cells) and the CTL response

97
Q

what are the bacterial strategies for resistance to phagocytosis?

A
  1. neutralization of the phagolysosome components: capsule, surface modification, proteases, peptidases, resistance to low pH
  2. resistance to reactive oxygen species: production of catalase, superoxide dismutase, surface polysaccharide and proteins that detoxify oxygen radicals
  3. prevention of phagolysosomal fusion
  4. escape from the phagosome
98
Q

how does legionella stop the acidification of the phagosome and the maturation process?

A

prevents acidification of the phagosome and eliminates phagosome surface proteins needed for the fusion with lysosomes

99
Q

how does salmonella prevent phagolysosomal fusion?

A

actively remodels the endosomes at an early stage of maturation (after invasion of M cells)

100
Q

how does mycobacterium tuberculosis (Mtb) prevent phagolysosomal fusion?

A

enters the phagocytes by binding to the receptor for activated C3b. It then recruits the host cell protein TACO, to the phagosome to block fusion with the lysosome
also prevents acidification, oxidative burst, and production of Il12 (Il12 normally activate Th1 response)

101
Q

What is dissemination?

A

the action of cell-to-cell spreading by producing actin, known as actin-based motility. allows pathogens to completely avoid the antibody-mediated response; there is no extracellular phase during infection.
polymerization of actin to push the bacterium forward

102
Q

dissemination also involves the production of ___ & ____ degradative enzymes to destroy cells

A

ECM (proteases, hyaluronidases) and toxins to destroy cells

103
Q

what is the significance of the production of plasminogen activator?

A

induces degradation of fibrin clots and allows the bacteria to escape blood clots (streptokinase)

104
Q

what does the production of DNAse do?

A

destroy NETs

105
Q

most bacteria require ___ for growth

A

iron

106
Q

what bacterial pathogen does not use iron for growth?

A

Borrelia burgdorferi - lacks all the iron-dependent cofactors and enzymes and uses MANGANESE instead of iron for the chemistry it needs for survival and replication

107
Q

what are siderophores?

A

small molecules that have a high affinity for iron, even higher than the host’s affinity

108
Q

what do siderophores do?

A

excreted out of bacterial pathogen’s membrane, acquires iron, and re-enters the bacterial cell by binding to the iron-siderophore receptor, and traveling back through a channel

109
Q

bacteria that are dependent on co-infection for the acquisition of iron do what?

A

produce receptors for siderophores produced by other bacteria

110
Q

besides producing siderophores and relying on other infections to be present, what else can bacterial pathogens do to acquire iron?

A

use the iron-binding protein of the host as a source of iron. bacterial receptors bind to the host iron-binding proteins (lactoferrin, transferrin)

111
Q

____ pathogen is able to take up iron directly from heme

A

staphylococcus aureus

112
Q

what is the benefit of pathogens inducing toxins inside the cell?

A

acquiring nutrients, evading the host immune system, or creating an optimal niche for growth

113
Q

what is BoNT, and what does it cause?

A

botulinum neurotoxin. causes flaccid paralysis which leads to death due to the collapse of the respiratory system

114
Q

why is it hard to understand the benefit of BoNT?

A

after the toxin enters the host, there is no infection of C. botulinum and the pathogen is rapidly eliminated from the body

115
Q

where are most toxin genes found?

A

on PAIs, prophages and other mobile genetic elements

116
Q

what is the major driving force in the evolution of toxins and toxin-producing bacteria?

A

HGT (horizontal gene transfer)

117
Q

what organisms are the likely targets of toxins, that happen to also affect humans?

A

animals, lower eukaryotes, insects and protozoa

118
Q

the C. diphteriae toxin is carried on a ____

A

prophage

119
Q

toxins are categorized based on their …

A

target, characteristics and structure, the disease they cause, and their mode of action

120
Q

two general categories of toxins

A
  1. endotoxin: part of the bacterial pathogen

2. exotoxin: secreted into the surrounding as the bacterial pathogen grows

121
Q

categorizations by mode of action:

A
  • type I toxin: binds to the target cell surface and acts extracellularly (ex. superantigen)
  • type II toxin: binds to the target cell surface and acts on the eukaryotic cell membranes
  • type III toxin: AB type toxin, binds to the target cell surface, enters the host cells, and activates or inactivates intracellular targets
122
Q

endotoxins (nonprotein)

A

integral membrane components of bacteria such as LPS, LTA/TA, and peptidoglycan. both in gram negative and positive bacteria.
released from bacterial cells during replication and when they lyse.
weakly antigenic but highly immunogenic
produce general systemic effects

123
Q

what is septic shock?

A

a state of multisystem organ hypofusion (low blood pressure) which deprives organs of nutrients and oxygen

124
Q

what bacterial infections usually cause septic shock?

A

septicemia

125
Q

what are the four clinical stages of septic shock?

A
  1. systemic inflammatory response syndrome (SIRS): fever or hypothermia, high heart rate and high respiratory rate
  2. Sepsis: SIRS + documented septicemia (presence of bacteria in the bloodstream)
  3. severe sepsis: organ dysfunction and low blood pressure. at this stage 70% of patients die
  4. septic shock: low blood pressure despite administration of fluid
126
Q

what is the mechanism of septic shock?

A

bacteria lyse, LPS are released, LPS bind to LPS binding protein, LPS and the LPS binding protein attach to the CD14 receptor on the macrophage inducing interleukins, activation of the complement cascade, and activation of the coagulation cascade

127
Q

what syndrome does activation of the coagulation cascade cause?

A

acute respiratory distress syndrome

128
Q

what toxin does Bordetella pertussis produce?

A

tracheal cytotoxin (TCT, peptidoglycan subunit)

129
Q

what does tracheal cytotoxin cause?

A

arrest of cilliary movement, cell death and release of IL-1 (pro-inflammatory) - cause of whooping cough

130
Q

what kind of toxin is the tracheal cytotoxin?

A

an endotoxin, nonprotein

131
Q

what kind of toxin is mycolactone?

A

an endotoxin, nonprotein

132
Q

what does Mycobacterium ulcerans cause?

A

buruli ulcers, a chronic infection leading to necrotic lesions

133
Q

mycolactone is a diffusable ___ toxin

A

lipid

134
Q

lesions caused by mycolactone are characterized by …

A

little inflammation and no physical pain

135
Q

what kind of pathogen is M. ulcerans?

A

an intracellular pathogen that grows inside the macrophages and in necrotic tissues

136
Q

what are type 1 exotoxins (protein toxins)? what do they do?

A

Superantigens: triggers uncontrolled, massive activation of T cells and APCs, leading to massive release of cytokines and shock

137
Q

what syndrome do superantigens cause?

A

toxic shock syndrome and food poisoning

138
Q

what is the cause of toxic shock syndrome?

A

tampons

139
Q

what are type II exotoxins (protein toxins)?

A

membrane-disrupting toxins

140
Q

what are the three different roles of membrane-disrupting toxins?

A
  1. kill host cells
  2. destroy the phagosome and enter the host cell cytoplasm
  3. exit cells after intracellular replication
141
Q

what are the two types of membrane-disrupting toxins?

A
  1. pore-forming toxins

2. phospholipase

142
Q

what do pore-forming toxins do?

A

forms a channel in the host membrane, leading to a sudden inrush of water and cell lysis

143
Q

what are the two types of pore-forming toxins?

A
  1. alpha-pore-forming toxins

2. beta-pore-forming toxins

144
Q

what do alpha pore-forming toxins do?

A

form alpha helices that penetrate the membrane

145
Q

what do beta pore-forming toxins do?

A

form beta sheets that form beta barrels in the membrane (requires oligomerization)

146
Q

what is an example of a pore-forming toxin?

A

streptolysin - comes from streptococcus pyogenes

147
Q

what bacteria use pore-forming toxins?

A

S. pneumoniae - toxin: pneumolysin

148
Q

what does phospholipase do?

A

destroys the integrity of the host cell membrane phospholipids - lysis of host cells

149
Q

what bacterial pathogen uses phospholipase?

A

listeria

150
Q

what are AB toxins?

A

type 3 exotoxins, composed of 2 subunits (enzymatic subunit A, binding/cell entry B)

151
Q

what does the A subunit of AB toxin do?

A

modifies a target inside the host cell leading to damage to the host

152
Q

what does the B subunit of AB toxin do?

A

binds to specific cell receptors providing tissue/cell type specificity

153
Q

how are the two subunits of the AB toxin linked?

A

covalent disulfide bond

154
Q

what is the bond between multisubunit AB toxin?

A

non-covalent interactions, which are disrupted when the toxin is internalized

155
Q

how do AB toxin cells enter the host?

A

endocytosis

156
Q

how is endocytosis mediated of AB toxins into the host cell?

A

endocytosis requires the passage of the A subunit through the membrane of the endosome, usually mediated by the B subunit

157
Q

how do anthrax toxins (a type of AB toxin), enter the host cell?

A

oligomerization of the B subunit on the surface of the host cell, binding of the A subunits to the B domain, and the endocytosis and passage of A subunits through the pore

158
Q

What is the effect of the Diphteria toxin?

A

colonizes the throat via C. diphteriae that carry the lysogenic corynebacteriophages. causes considerable damage to the mucosa of the throat and also cause skin infections via wounds

159
Q

what does ADP-ribosylation cause?

A

inactivation of the protein or a change in its activity

160
Q

what toxin catalyzes ADP-ribosylation of host cell proteins?

A

the A subunit of the AB toxin

161
Q

what are the two targets of ADP ribose during ADP-ribosylation?

A
  • EF-2: stop protein elongation (death)
  • Gs protein: regulates cyclic AMP levels, cell loses control of ion flow and results in massive loss of water when ADP ribose binds to the protein
162
Q

What bacterium causes botulism?

A

Clostridium botulinum, anaerobe

163
Q

how does botulism spread?

A

germination of C. botulinum’s spores

164
Q

what is the toxin produced by botulism?

A

BoNT - neurotoxin

165
Q

what are the characteristics of BoNT?

A
  • 7 serotypes
  • very potent: lethal dose is 1-5 ng/kg
  • recovery takes 4-6 months
166
Q

what are the three types of botulism?

A
  1. food-borne botulism
  2. infant botulism
  3. wound botulism
167
Q

what is the mode of action of BoNT?

A
  1. BoNT binds to the motor neuron receptor, specifically the heavy chain to the receptor, and endocytosis into the motor neuron
  2. LC, an endoprotease that is part of BoNT, is translocated from the vesicle via the N-terminal portion of the heavy chain which forms a channel in the vesicle membrane, into the cytoplasm of the motor neuron
  3. LC then cleaves SNARE proteins which prevents Acetylcholine being released into the muscle cell - this process prevent muscle contraction, i.e., flaccid paralysis
168
Q

LC’s from different BoNT ___ target different ___ proteins

A

serotypes

SNARE

169
Q

What is tetanus?

A

an infection coming from clostridium tetanii, found in the soil as a spore

170
Q

what is the impact of the toxin, TeNT, that tetanus produces?

A

enters the blood stream, acts on the neurons, causing spastic paralysis, i.e., constant muscle contraction

171
Q

what is the mechanism of TeNT?

A

targets inhibitory synapses of the CNS and undergoes retrograde transport to the inhibitory neuron

172
Q

what happens during TeNT transcytosis?

A

TeNY inhibits Glycine secretion so the contracted muscles never receive a signal to stop muscle contraction

173
Q

what specific SNARE protein does TeNT affect?

A

VAMP2

174
Q

what is the treatment of tetanus?

A
  1. vaccination
  2. antitoxin (passive immunization)
  3. antibiotics + cleaning of the wound
  4. muscle relaxant + curare (block the Ach receptor)
175
Q

what are secretion systems?

A

virulence factors of bacteria, that allow the bacteria to interact with and modify their surrounding environment. secretion systems also allow bacteria to transport virulence proteins (toxins)

176
Q

what is the role of protein secretion systems?

A

transports adhesins (surface factors), toxins, exoenzymes, proteases, and other virulence factors onto the cell surface, for release into the medium and direct delivery inside the host cells

177
Q

the protein secretion system of gram-negative bacteria are more ___, more ___, and more ____ than those of gram-positive bacteria

A

numerous
complicated
diverse

178
Q

what is the basic secretory system (Sec system)?

A

a secretion system used by both gram-negative and gram-positive bacteria to translocate proteins across the cytoplasmic membrane

179
Q

the Sec system transports ___ proteins

A

unfolded

180
Q

where is the signal sequence located on proteins that are transported via the Sec system?

A

N-terminus

181
Q

what are the proteins involved in Sec system?

A

SecB, SecA, SecYEG, SecDF, YajC

182
Q

what is the function of SecB?

A

a chaperone that binds to signal sequences and keeps the protein to be secreted in an unfolded state

183
Q

what is the function of SecA?

A

is an ATPase that provides some of the energy needed for translocation. the proton motive force or translocation provides the rest of the energy needed.

184
Q

what complex do the SecYEG proteins make up?

A

the heterotrimeric complex

185
Q

what is the role of the heterotrimeric complex?

A

forms a protein-conducting channel through the cytoplasmic membrane

186
Q

what is the function of SecD, SecF, and YajC?

A

help to stabilize the whole complex

187
Q

what is the overall mechanism of the Sec system?

A

SecB transports the unfolded protein to SecA where it’ll be translocated across the membrane through the heterotrimeric complex (SecYEG proteins). YidC attaches the the heterotrimeric complex to act as an accessory protein that helps translocation. After the unfolded protein is exported, it attaches to SPase, located in the membrane, and where it is cleaved.

188
Q

what is the Twin-arginine transport (TAT) system?

A

secretory system used by both gram-negative and gram-positive bacteria to translocate FULLY FOLDED proteins to the periplasm / surrounding medium

189
Q

how is energy provided in the TAT system?

A

proton motive force across the membrane

190
Q

what are secretion systems specific to gram-negative bacteria?

A

secretion systems used to cross the outer membrane

191
Q

what are the two categories of secretion systems specific to gram-negative bacteria?

A
  1. sec-dependent
    • type 2, type 5
  2. sec-independent
    • type 1, 3, 4, 6
192
Q

what is the type 2 secretion system (T2SS) and what is its general mechanism?

A

also known as the general secretion pathway. unfolded proteins transported into the periplasm via the Sec pathway, followed by the protein PulA being secreted by T2SS.

193
Q

how are cholera toxins secreted through the T2SS?

A

A and B subunits are translocated separately from each other via the Sec system, followed by the formation of the toxin (bonding of A and B subunits) in the periplasm. the resulting cholera toxin is then translocated across the outer membrane via PulD and PulS protein complex

194
Q

what is the Type 5 secretion system?

A

an auto transporter that transports itself across the outer membrane (the protein transports itself)

195
Q

what is the makeup of the T5SS?

A

a large multi domain protein, including a Sec signal sequence, a beta domain, and other domains such as alpha, gamma, and sometimes a protease

196
Q

the overall mechanism of T5SS?

A

protein is auto transported using the N-terminal signal sequence, entering the periplasm where it then travels through the beta domain of the T5SS and autocleaves it self into two parts (alpha and gamma), released from the outer membrane

197
Q

what is the function of T1SS?

A

translocates protein directly from the cytoplasm to the cell surface, bypassing the Sec system and the periplasm

198
Q

in what state are proteins translocated via the T1SS?

A

unfolded

199
Q

what is the inner membrane component of the T1SS and what is its function?

A

an ATP binding cassette (ABC) transporter that serves as a channel in the cytoplasmic membrane. it supplies energy to the whole system

200
Q

what is the signal sequence of T1SS?

A

C-terminal signal sequence consisting of a glycine-rich sequence repeated up to 36 times

201
Q

what bacterial pathogen uses T1SS?

A

E. Coli - secretes alpha hemolysin

202
Q

what is the outer membrane component of T1SS made up of?

A

a channel made of three monomers

203
Q

what is the function of the Type 3 secretion system?

A

forms a channel through the bacterial cytoplasmic membrane, the periplasm, the outer membrane, and the host cell membrane so bacterial proteins can be injected into the host cell cytosol

204
Q

what category of bacteria uses Type 3 secretion system?

A

a large number of gram-negative bacteria

205
Q

what are T3SS effectors?

A

bacterial toxins transported by the T3SS - no B subunit because the specificity and transport is provided by the T3SS itself

206
Q

what is the make-up of T3SS?

A

made of 3 channel complexes, one for each membrane it crosses. subunits must be transported in a chronological order: bacterial channel, needle, needle extension, translocation pore - effectors are then directly transported into the host cytoplasm

207
Q

what bacterial pathogen uses T3SS?

A

Yersinia pestis - using this secretion system avoids the antibody-mediated immune response

208
Q

what system is T3SS similar to?

A

the flagellar assembly system

209
Q

what is the function of the T4SS?

A

translocates proteins and DNA in a contact-dependent and ATP-driven manner. very tight contact is needed

210
Q

where is the T4SS sometimes found?

A

on PAI’s

211
Q

what is the make up of T4SS?

A

12 proteins that form a complex that span the 2 membranes of the bacteria. this system is related to the tra conjugal-transfer system used to transfer plasmid DNA

212
Q

what bacterial pathogen largely uses T4SS?

A

L. pneumophila

213
Q

what is the function of T6SS?

A

directly injects proteins into the host cells in a contact-dependent, ATP-driven mechanism. can also deliver toxins into other bacterial cells.

214
Q

T6SS has a structural similarity with …

A

bacteriophage tail proteins - may have originated from a defective prophage

215
Q

what is the function of outer membrane vesicles?

A

eliminate toxic compounds and misfolded proteins. can also be used to transfer toxins into host cells via fusion of the OMV with the host cell.

216
Q

what secretion systems are specific to gram-positive bacteria?

A

cytolysin-mediated translocation (CMT) (sec-dependent) and T7SS (sec-independent)

217
Q

what is the main difference between sec systems in gram-positive and gram-negative bacteria?

A

sec systems in gram-positive bacteria do not involve a periplasm or an outer membrane because they do not exist in gram-pos.

218
Q

what is the function of cytolysin-mediated translocation (CMT)?

A

secretes pore-forming toxins in to the host cytoplasm, creating a pore in the host membrane. this allows other bacterial proteins, such as toxins, to enter the host cells

219
Q

an ____ binds to the host cell and ensures that the sec-system and the cytolysin are correctly aligned

A

adhesin

220
Q

what is the T7SS particularly efficient for?

A

rapidly transporting bacterial toxins across the bacterial membrane and cell envelope of Mycobacterium and Gram positive

MICR 341 - Quiz 4 (2 decks)

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