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Infectious Disease Final > Lecture 7 Part 2 > Flashcards

Lecture 7 Part 2 Flashcards

1
Q

what is the term for multiple ribosomes binding to a single mRNA?

A

polyribosome

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2
Q

explain the ribosomes of prokaryotes

A

30s and 50s

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3
Q

what is the first amino acid in protein translation in a prokaryote

A

N-formyl methionine

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4
Q

what are the 2 sites in a prokaryotic ribosome, important in bacterial protein translation?

A

p site (peptidyl transferase)
a site (aminoacyl

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5
Q

in order for bacterial protein translation to begin, what has to happen?

A

N-formyl methionine has to bind to a very specific tRNA that will bind in the P site of the ribosome

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6
Q

bacteria express their genes in groups by means of ____ rather than _____

A

by means of OPERONS rather than using individual promoters for each gene

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7
Q

true or false

in a bacterial operon, if gene expression is stimulated for 1 gene, ALL genes in the operon get expressed

A

TRUE

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8
Q

TRUE OR FALSE

transcription and translation happens simultaneously in bacteria and uses the same enzyme

A

TRUE (enzyme = RNA polymerase)

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9
Q

name 4 ways in which operon can be turned “OFF”

A
  1. Repressor protein binds and blocks transcription
  2. activator protein does not bind its inducer and thus cannot bind to the promoter region
  3. repressor protein binds its corepressor and is able to bind and block transcription
  4. inhibitor binds to activator protein, preventing it from binding to promoter region
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10
Q

“negative control of an inducible gene”

A

gene is off unless repressor protein binds inducer

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11
Q

“negative control of a repressible gene”

A

gene is on unless repressor binds its corepressor

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12
Q

“positive control of an inducible gene”

A

gene is off unless activator binds its inducer

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13
Q

“positive control of a repressible gene”

A

gene is on unless inhibitor binds to activator

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14
Q

MUTATIONS change what?

A

the base pair sequencw

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15
Q

what is the difference between transition and transversion?
which is more danegrous?

A

transition – pyrimidine to pyrimidine (C to T) or purine to purine (G to A)

transversion – purine replaced by pyrimidine or pyrimidine replaced by purine

TRANSVERSION is more dangerous

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16
Q

these 4 terms reflect the change to the amino acid as a result of mutations:

A

-silent
-missense
-frameshift
-null

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17
Q

what is a missense mutation?

A

single nucleotide change that results in coding for a different amino acid

types of missense mutations:
-conservative (protein will still function)

-nonconservative (changing of charge or hydrophobicity)

-nonsense mutation — results in stop codon. could still result in an active or partially active protein

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18
Q

what is a frameshift mutation?

A

insertion or deletion of a nucleotide that throws the coding region out of frame

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19
Q

what is a null mutation?

A

results in a protein that does not function properly or no creation of the protein at all

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20
Q

name 2 ways in which bacterial genetic material can be exchanged

A

-through plasmids – when plasmid DNA replicate along with the bacterial genome

-through bacteriophages (bacterial viruses). they can transfer genetic material (virulence genes) to bacteria

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21
Q

_________ elements allow the transfer of bacterial genetic material

A

extrachromosomal genetic elements

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22
Q

the transfer of bacterial genetic material can cause the creation of what?

A

a new bacterial strain

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23
Q

name the 4 ways in which bacteria can exchange genetic information

A

transformation and transduction

transformation – donor cell lyses and releases their DNA fragments into the recipient cell, which then integrates into plasmids

transduction – cell containing bacteriophages lyses and releases phages. they infect the host cell (inject their DNA?) where they integrate DNA with the host

conjugation – free PLASMID moves from donor to recipient via sex (F) pilus. the integrated plasmid then promotes the transfer of genomic DNA which then integrates into recipient DNA as well

transposition– movement of DNA elements WITHIN THE CELL (can be a virulence island)

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24
Q

the severity of disease due to bacterial infection depends on what 5 factors?

A

-the tissue or bodily function affected

-the strain of bacteria

-inoculum size

-the threshold for disease production

-susceptibility of the host

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25
Q

the strength of the response to infection (actions of the immune system to fight it) depend on what 4 things?

A

-the duration of the infection

-the number of pathogens

-the ability of the pathogens to colonize

-the damage potential

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26
Q

bacteria have 8 virulence factors. name all 8

A

adherence

invasion

encapsulation

metabolic byproducts

toxins

excess inflammation (cytokine storm)

evasion of immune response

resistance to antibiotics

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27
Q

how can bacteria adhere to the host membrane?

A

through attachment proteins or pilli binding to membrane host receptors

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28
Q

are pathogenicity islands chromosomal or extrachromosomal?

A

extrachromosomal

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29
Q

what is the function of RNA III on pathogenicity islands

A

RNA III can down regulate adhesion genes and up regulate the production of biofilm and toxins. (all has to do with where the complementary is

it does this through interaction with mRNA. RNA III and mRNA can base pair (if complementary) to form a double helix

30
Q

which specific bacteria used RNA III to control virulence genes in its pathogenicity islands?

A

staphylococcus aureus

31
Q

explain the process of the staphylococcus aureus pathogenicity island

A

AGR gene is phosphorylated and stimulates the phosphorylation of AGRA gene. this then activates and phosphorylates the transcription factor called SarA —

SarA causes the transcription of these AR genes and also causes the transcription of RNA III which regulates adhesion/biofilm/toxin genes

32
Q

what is chromosomal integration?

A

when a virulence gene from one bacteria is transferred to another

33
Q

name the 4 major steps of bacterial infection

A

-entry

-colonization

-destroy

-evade

34
Q

name 2 ports of entry for bacteria

A

-natural openings (ie mouth, conjunctiva)

-barrier breaches (ie: scratches)

35
Q

is their normal flora in the skin?

A

yes – just a little

36
Q

in which 4 places do we have the MOST flora

A

oropharynx
upper respiratory tract
intestinal tract
vagina

37
Q

name some natural immune defenses

A

mechanical barrier

ciliated epithelium

normal flora

mucus

sIgA

lymhpoid follicles

low pH

flushing effects (big in conjunctiva)

peristalsis

38
Q

true or false

bacteria MUST bind to host cell surfaces

A

true

39
Q

what is another word for pili

A

fimbriae

40
Q

besides pili, what other bacterial proteins can act as adhesins and interact with host receptors?

A

proteins in bacterial cell well (ie: lipoteichoic acid)

41
Q

bacteria can colonize via ___ production

A

BIOFILM

42
Q

describe the structure and function of biofilm

A

-composed of polysaccharides

biofilm protects the bacteria colony from host defenses and antibiotics. it binds the cells of a colony together, and is produced when the colony number reaches a certain threshold (quorum)

43
Q

give an example of a natural biofilm

A

dental plaque

44
Q

3 methods of bacterial colonization

A

-destroy host barrier

-effector proteins facilitate the transport of bacteria

-transportation of bacteria via m cells

45
Q

“effector proteins can facilitate the transport of bacteria”

give 2 specific examples

A

-E. coli secretes proteins that form a docking station

-salmonella secretes proteins that promote vesicular uptake into host cells

46
Q

how do bacteria transport across mucus membranes?

A

through M cells

47
Q

name 3 bacterial metabolic byproducts that are toxic to eukaryotic cells

A

acids
gases
(other)

48
Q

what do virulence factors do?

A

increase the pathogenicity

49
Q

name 3 bacterial degradative enzymes

A

-collagenase

-hyaluronidase

-fibrinolysin

50
Q

what does hyaluronidase do?

A

break outer cell membranes of the host

51
Q

name 2 cell death mechanisms caused by bacteria

A

apoptosis and lysis

52
Q

how can bacteria indirectly cause destruction?

A

excessive immune response (inflammatory response)

53
Q

which type of bacteria (gram positive or gram negative) produce exotoxins?

A

BOTH

54
Q

exotoxins are often encoded on ___ or ____

A

plasmids or bacteriophages

55
Q

give 4 examples of exotoxins

A

-degradative enzymes
-hemolysins
-cytolytic toxins
-pore-forming toxins

56
Q

what makes exotoxins expecially bad?

A

they are often able to move from bacteria to bacteria

57
Q

give an example of a pore-forming toxins and a cytolytic toxin

A

pore-forming: streptolysin

cytolytic: alpha toxin

58
Q

many exotoxins are ____, meaning what?

A

DIMERIC – A-B toxins

B subunit binds cell surface receptor while A subunit is transferred into the host cell to do damage

59
Q

explain what pore-forming exotoxins do

A

create a pore in the host plasma membrane. the cytoplasmic contents leave the host cell and water rushes in, causing swelling and then cell lysis

60
Q

which toxin irreversibly blocks EF-2?
what kind of toxin is it?
explain how it works

A

Diphtheria toxin – A-B toxin.

b subunit binds to cell membrane. A subunit goes into the cell and enzymatically inactivates EF-2, which prevents protein synthesis at the host ribosome. this causes cell death

VERY POWERFUL enzymatic reaction. just 1 molecule is sufficient to shut down all ribosomes

61
Q

which toxin causes the overproduction of cAMP? what kind of toxin is it?
explain how it works

A

Cholera toxin – A-B toxin
A2B5 toxin. B binds to a “ganglioside receptor” and A1 and A2 enter the cell (only A1 is active)

A1 causes increased adenylate cyclase activity, which causes the overproduction of cAMP, and thus the export of many nutrient ions. cell dies. diarrhea occurs due to the flow of ions + water leaving the cell

62
Q

which toxin blocks the release of inhibitory neurotransmitter? what kind of toxin is it?
explain how it works and what is causes

A

tetanus toxin – A-B toxin

blocks the release of inhibitory neurotransmitter, causing continuous excitation. chronic stimulation of the nerve

63
Q

which toxin causes paralysis? what kind of toxin is it?
explain how it works

A

botulinum toxin

blocks the release of acetylcholine at neuromuscular junction. cant stimulate the muscle. paralysis

64
Q

what do superantigens do?
explain in detail

A

superantigens simultaneously bind T-cell receptors and MHC class II. This activates a lot of T cells and induces CYTOKINE STORM – all in absense of an actual antigen. Both the T cell and MHC class II chronically producing cytokines

causes auto-immune responses (Toxic shock syndrome). and can lead to T cell apoptosis

65
Q

give examples of endotoxins/endo-like toxins

A

the cell wall components of bacteria.

ie: LPS lipid A on gram negative – highly toxic

lipoteichoic acid and peptidoglycan on gram positive bacteria (endotoxin-like)

66
Q

explain how endotoxins function

A

they are recognized by immune cell receptors (ie: macrophages, neutrophils, B cells, TLRS, CD14)

This stimulates the acute phase cytokine production (IL-1 IL-6 TNFa) which can affect coagulation and causes B cell proliferation. HIGH LEVELS OF ENDOTOXIN CAN LEAD TO TOXIC SHOCK (overproduction of cytokines)

67
Q

antibodies to LPS are made to which portion?

A

the O side chain

68
Q

why is LPS a very effective endotoxin

A

it induces a lot of responses and overproduction of cytokines – leads to toxic shock/DIC thrombosis (abnormal clots inside blood vessels)

69
Q

name 7 ways in which bacteria can evade the immune system

A

-encapsulation (hide LPS or lipoteichoic acid in capsule)

-antigenic mimicry (modify LPS)

-prevent complement fixation (through C3 peptidase – breaks down C3)

-inhibit phagocytosis

-replicate INSIDE CELL (avoid detection)

-immunosuppression (avoid destruction)

-produce superantigens (excessive activation of immune system. the body is distracted from the actual infection and just keeps producing cytokines)

70
Q

name 4 methods that bacteria use to inhibit phagocytosis

A

-inhibit the RECRUITMENT of phagocytes

-avoid recognition by macrophages (pose as self)

-induce macrophage death

-inhibit the function of lysosomes

71
Q
A

Infectious Disease Final (13 decks)

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