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STEP > ID 3 > Flashcards

ID 3 Flashcards

1
Q

Function of type III secretion system?

A

facilitates direct delivery of toxins from certain gram negatives to eukaryotic host cells.

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2
Q

bugs with type III secretion systems?

A

1) pseudomonas
2) salmonella
3) shigella
4) e coli

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3
Q

other name for transformation?

A

competence

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4
Q

bugs with transformation ability

A

1) s pneumo
2) H flu
3) neisseria

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5
Q

How can you prevent transformation?

A

add deoxyribonuclease.

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6
Q

F+ means?

A

Has genes required for sex plus and conjugation

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7
Q

What is transferred through piles in conjugation?

A

Single strand of plasmid DNA. NO chromosomal DNA.

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8
Q

Hfr cell?

A

Cell that has incorporated F+ plasmid into bacterial chromosomal DNA.

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9
Q

Caveat about Hfr Cells

A

When plasmid DNA is replicated, some flanking chromosomal DNA can be replaced. Thus, Hfr cells can transfer BOTH plasmid and chromosomal genes.

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10
Q

transposition occurs?

A

Between plasmid and chromosome and vice versa

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11
Q

transposition caveat

A

flanking chromosomal DNA can be transferred to another bacterium

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12
Q

example of transposition

A

vanA gene transferred from VRE to S aureus

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13
Q

Generalized transduction

A

A “packaging” event. Lytic phage infects bacterium, leading to cleavage of bacterial DNA. Parts of bacterial chromosomal DNA may become packaged in phage capsid. Phage then infects another bacterium –> genes transferred.

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14
Q

Specialized transduction

A

“Excision event.” Lysogenic phage infects bacterium; viral DNA incorporates into bacterial chromosome –> phage DNA excised –> flanking bacterial genes may be excised with it –> DNA is packaged into phage capsid and can infect another bacterium.

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15
Q

Genes from what toxins are encoded in a lysogenic phage?

A 
ABCD's
Group A strep erythrogenic toxin
Botulinum toxin
Cholera toxin
Diphtheria toxin
Shiga toxin
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16
Q

when do bacteria form spores?

A

End of stationary phase

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17
Q

how do you kill spores?

A

autoclave by steaming at 121 C for 15 minutes.

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18
Q

Exotoxin composition?

A

polypeptides

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19
Q

where are exotoxin genes?

A

plasmid or bacteriophage

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20
Q

potency of exotoxins vs. endotoxins

A

Exotoxins are VERY dangerous (fatal dose on order of 1 microgram)
Endotoxins are less potent (fatal dose on order of hundreds of micrograms)

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21
Q

antigenicity of exotoxins?

A

Induces high-titer antibodies called antitoxins.

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22
Q

what is titer?

A

way of expressing concentration

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23
Q

vaccines against exotoxins?

A

toxoids

24
Q

heat stability of exotoxins?

A

Destroyed rapidly at 60 degrees C (except staphylococcal enterotoxin)

25
Q

typical exotoxin diseases

A

1) tetanus
2) botulism
3) diphtheria

26
Q

source of endotoxins?

A

outer cell membrane of gram negatives

27
Q

composition of endotoxins?

A

Lipid A component of LPS

28
Q

Effects of endotoxins?

A

1) fever
2) shock
3) *DIC

29
Q

cytokines induced by endotoxin?

A

TNF
IL-1
IL-6

30
Q

are endotoxins antigenic?

A

poorly antigenic

31
Q

vaccines for endotoxin?

A

none available

32
Q

heat stability of endotoxin?

A

stable at 100 degrees C for 1 hr

33
Q

endotoxin diseases?

A

1) meningococcemia

2) sepsis by gram negative rods

34
Q

Effect of diphtheria toxin?

A

1) pharyngitis with pseudomembranes in throat

2) severe lymphadenopathy (bull neck)

35
Q

name of pseudomonas toxin?

A

exotoxin A

36
Q

shigella toxin

A

Shiga toxin (ST)

37
Q

Shiga toxin mechanism

A

Inhibits protein synthesis by inactive 60S ribosome by removing adenine from rRNA

38
Q

EHEC toxin

A

Shiva-Like toxin (SLT)

39
Q

shiga-like toxin mechanism

A

inhibits protein synthesis, same as shigella

40
Q

What else can shigella cause other than dysentery?

A

hemolytic-uremic syndrome (HUS) (same toxin)

41
Q

difference between shigella and EHEC?

A

EHEC doesn’t invade host cells

42
Q

SLT and HUS mechanism?

A

SLT enhances cytokine release

43
Q

Heat-labile toxin (LT) MOA

A

Over activates adenylate cyclase (increasing cAMP) –> increasing Cl secretion in gut and H2O efflux

44
Q

heat-stable toxin (ST) MOA

A

over activates guanylate cyclase (increasing cGMP) –> decreasing resorption of NaCl and H2O in gut.

45
Q

name of anthrax toxin

A

edema toxin

46
Q

MOA of edema toxin?

A

Mimics adenylate cyclase enzyme, increasing cAMP, and *increasing fluid secretion. This explains the edematous borders of black eschar in cutaneous anthrax.

47
Q

cholera toxin MOA

A

Overactivates adenylate cyclase (increasing cAMP) by permanently activating Gs –> increasing Cl- secretion in gut and H2O efflux.

48
Q

Pertussis toxin MOA

A

Over activates adenylate cyclase (increasing cAMP) by disabling Gi, impairing phagocytosis to permit survival of microbe.

49
Q

caveat about whooping cough

A

toxin may not actually be a cause of cough

50
Q

name of tetanus toxin

A

tetanospasmin

51
Q

tetanospasmin and botulinum toxin MOA

A

proteases that cleave SNARE. **both inhibit release of neurotransmitter.

52
Q

What is SNARE?

A

soluble NSF attachment protein receptor

53
Q

cells impaired by tetanus

A

Renshaw cells (which contain GABA and glycine)

54
Q

AB toxins

A

1) diphtheria
2) exotoxin A of pseudomonas
3) shiga toxin
4) shiga-like toxin
5) Heat-*labile toxin
6) edema toxin
7) cholera toxin
8) pertussis toxin
9) tetanospasmin
10) botulinum

55
Q

AB toxin structure

A

B enables binding, A is usually ribosyltransferases

STEP (85 decks)

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