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MICRO 442 > MIrocm 442 Ch 5-7 > Flashcards

MIrocm 442 Ch 5-7 Flashcards

1
Q

Includes external defenses and internal defenses

A

innate immunity (1st line of defense)

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2
Q

-primary response takes time
-targeted to specific microbes
-clonally rearranged receptors
-immunologic memory

A

adaptive immunity (takes days initially)

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3
Q

-physical and chemical barriers
-mucous membranes

A

external defenses

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4
Q

-complement
-phagocytic cells
-pattern recognition receptors
-inflammatory response

A

internal defenses

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5
Q

-antibodies via plasma cells
-cell-mediated response (t-cells)

A

humoral response

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6
Q

thick layer of dead cells in the epidermidis

A

skin

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7
Q

contain lysozyme, which digests peptidoglycan

A

tears

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8
Q

antibacterial enzymes

A

saliva

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9
Q

mucus and cilia trap and remove organisms

A

respiratory

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10
Q

-mucus=viscous, contains antimicrobial properties
-inner mucus=essentially sterile
-cell surface mucins prevent pathogen binding

A

GI tract mucosa

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11
Q

thick due to secretions

A

mucus

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12
Q

most bacteria in GI tract is in

A

outer layer

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13
Q

secrete gel-forming mucins

A

goblet cells

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14
Q

secrete antimicrobial defensins and other proteins

A

paneth cells

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15
Q

transport antigens from gut lumen to cells of immune system

A

M-cells

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16
Q

the 3 pathways of complement activation

A

classical, lectin, and alternative

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17
Q

links innate and adaptive arms of the immune system -> antigen-antibody complexes

A

classical

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18
Q

mannose-binding lectin, lectin=protein that binds to sugar, recognizes bacterial sugars

A

lectin

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19
Q

pathogen surfaces -> biophysical characteristics of pathogen surface allows inactivation of complement

A

alternative

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20
Q

outcomes of complement activation

A
  1. inflammation and chemotaxis
  2. osponization (removal of pathogens)
  3. pathogen lysis (membrane attack complex)
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21
Q

genetic deficiencies in terminal complement components predispose to…

A

Nisseria infections

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22
Q

osponization targets

A

particles for uptake or phagocytosis but osponization-independent mechanisms can also trigger uptake

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23
Q

neutrophils have both

A

complement and antibody receptor to perform phagocytosis

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24
Q

ROS helps

A

the phagolysosome by binding to it and helping degrade bacteria

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25
Q

NADPH oxidase (which produces ROS) deficiency causes

A

chronic granulomatous disease

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26
Q

PRR are present

A

-on the cell surface
-in intracellular compartments
-in the cytoplasm

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27
Q

PRR bind to

A

PAMPs

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28
Q

Lipoproteins on GP bacteria

A

TLR1 and TLR2

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29
Q

LPS and GN

A

TLR4

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30
Q

flagellin and GN

A

TLR5

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31
Q

DNA on both GP and GN

A

TLR9

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32
Q

TLR signaling cascade leads to

A
  1. cellular activation
  2. cytokine production
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33
Q

Bacteria avoid TLR by

A

-modulating structures to prevent recognition
-interfering with signaling pathways

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34
Q

Inflammoses are in the

A

cytoplasm

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35
Q

-multi-protein innate immune sensing complexes
-have sensor proteins that detect conserved PAMPs and danger signals

A

Inflammoses

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36
Q

pro-inflammatory programmed cell death

A

pyroptosis

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37
Q

activate the protease caspase-1 and related proteases to activate cytokines and initiate pyroptosis

A

Inflammoses

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38
Q

cytokines cause

A
  1. vasodilation
  2. increase vascular permeability
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39
Q

inflammatory cells migrate into

A

tissue

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40
Q

B cell receptors/antibodies have

A

4 components
-light chain + heavy chain = variable region
-constant region = part of heavy chain

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41
Q

3 functions of antibodies

A
  1. neutralization
  2. osponization
  3. complement activation
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42
Q

T-cell receptor DNA is

A

rearranged and creates a dimer

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43
Q

cytosolic pathogen peptides bind to

A

MHC class I and presented to CD8 T-cells

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44
Q

extraceullular pathogen peptides bind to

A

MHC class II and presented to CD4 T-cells

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45
Q

CD4 helper t-cells

A

activate B cells & macrophages, produce cytokines

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46
Q

CD8 cytotoxic t-cells

A

kill infected cells and produce cytokines

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47
Q

agent characteristics

A

-virulence, dose, toxicity
-ability to survive in different environments
-antibiotic susceptibility

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48
Q

agent interventions

A

control/eliminate the infection at its source

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49
Q

Host characteristics

A

-behavior (age, sex, sexual practices, hygiene)

50
Q

host susceptibility

A

-genetics
-immunological status
-anatomic structure
-disease or medications

51
Q

host interventions

A

-treat infection
-immunize
-behavior modification

52
Q

environment characteristics

A

-place, geology, climate
-biologic factors -> insects transmit the agent
-socioeconomic factors -> crowding, sanitation, access to healthcare

53
Q

environment interventions

A

-sanitation, water
-preventive services
-spray to reduce mosquitoes
-bed nets

54
Q

resevoir

A

environment in which the infectious agent normally lives, grows and multiplies

55
Q

environmental reservoirs

A

-plants
-soil
-water

56
Q

skin to skin, kissing, sex, contact with soil/vegetation, droplet spread (sneezing/coughing)

A

direct transmission

57
Q

airborne (measles can live in air for hours), vehicle borne, vector borne

A

indirect transmission

58
Q

food, water, fomites

A

vehicle-borne transmission

59
Q

mosquitoes, fleas, ticks

A

vector-borne transmission

60
Q

reproduction number (how many people can 1 person infect)

A

R-naught (R0)

61
Q
  1. infectious period
  2. mode of transmission
  3. contact rate (location, public health measures, not specific to a disease)
A

factors for R-naught calculation

62
Q

observed>expected at a particular time and place

A

outbreak

63
Q

used to generate a DNA fingerprint for a bacterial isolate, bacteria from same strain will be indistinguishable -> gold standard

A

PFGE

64
Q

individual gene or whole genome

A

sequencing

65
Q

to establish link need not only DNA relatedness but

A

epidemiological connection

66
Q

natural or innate properties

A

intrinsic resistance

67
Q

-mutation
-horizontal gene transfer
-often under selection pressure

A

acquired resistance

68
Q

-efflux pumps
-permeability barriers
-target bypass

A

intrinsic resistance examples

69
Q

-efflux pumps
-inactivate the antibiotic
-modify the antibiotic target

A

acquired resistance examples

70
Q

-transformation
-conjugation
-transduction

A

types of horizontal gene transfer

71
Q

taking up free dna from environment

A

transformation

72
Q

transfer from one bacterium to another (plasmids/mobile elements)

A

conjugation

73
Q

bacteriophage infection -> phage picks up dna during infection and inserts it into another cell

A

transduction

74
Q

biofilms make it hard for antibiotics to

A

reach the target bacteria

75
Q

-metabolic byproducts
-reduced oxygen
-differences in pH
-some antibiotics sensitive to these changes

A

altered microenvironment in communities

76
Q

-subpop. go metabolically dormant
-antibiotics=less effective
-revert back to normal later

A

bacterial persister cells

77
Q

-exoplysaccharides, proteins, dna
-hard for antiobiotics to penetrate

A

sticky and slimy matrix of communities

78
Q

beta-lactams

A

cell wall inhibitors

79
Q

glycopeptides

A

cell wall inhibitors

80
Q

fluoroquinolones

A

dna targeting

81
Q

macrolides, lincosamides

A

ribosomal inhibitors

82
Q

tetracyclines

A

ribosomal inhibitors

83
Q

aminoglycosides

A

ribosomal inhibitors

84
Q

2 main enzymatic steps in cell wall synthesis

A
  1. crosslinked via stem peptides
  2. polymerized into glycan strands
85
Q

-nitromidazoles
-rifampin
-sulfonamides
-polymyxins

A

other processes of antibiotic classes

86
Q

transpeptidase

A

PBP that crosslinks

87
Q

glycosyltransferase

A

PBP that polymerizes

88
Q

different bacteria can have…

A

both or one of the PBPs

89
Q

what inhibits the transpeptidase activity of the PBPs

A

beta-lactams -> form a complex and PBPs can no longer crosslink -> cell wall integrity compromised

90
Q

-penicillins
-cephalosporins (start with ceph)
-carbapenems (end in penem)
-monobactems
-beta-lactam/beta-lactamse inhibitors
-cefiderocol

A

classes/subclasses of beta-lactams

91
Q

cefiderocol + carbapenems

A

broad-spectrum

92
Q

1-5 generations

A

cephalosporins

93
Q
  1. producing beta-lactamases to hydrolyze/inactivate the antibiotic
A

beta-lactams resistance mechanisms

94
Q

-amoxicillin/clavulanate
-ampicillin/sulbactam
-piperacillin/tazobactam

A

combination drugs with beta-lactamases

95
Q

beta-lactamases common in

A

GN -> chromosomal or plasmid-encoded beta-lactamases e.g. e.coli and klebsiella

96
Q
  1. mutating PBPs to lower the affinity for the antibiotic e.g. MRSA
A

beta-lactams resistance mechanisms

97
Q

-acquired mecA gene from mobile genetic element integrates into chromosome
-mecA encodes an alternative PBP2 protein called PBP2s
-reduced affinity for methicillin and other similar beta-lactams

A

MRSA

98
Q
  1. efflux pumps move the antibiotic out of the cell (see ya!)
A

beta-lactams resistance mechanisms

99
Q
  1. prohibiting entry by decreasing membrane permeability
A

beta-lactams resistance mechanisms

100
Q

vancomycin -> bind peptidoglycan D-ala D-ala dipeptide to block Tpase crosslinking

A

glycopeptide

101
Q

-used as a broad spectrum drug against GP
-too large to pass outer membrane (intrinsic resistance)

A

vancomycin

102
Q

-horizontal gene transfer that encodes for D-ala D-lactate ligase
-vancomycin doesn’t recognize anymore

A

VRE (vancomycin-resistant enterococcus)

103
Q

end floaxin

A

fluoroquinolones

104
Q

relax/unwind over-twisting positively supercoiled DNA by cleaving and reuniting the strands

A

type II topoisomerases, dna gyrase and topoisomerases IV in fluoroquinolones

105
Q

-target site mutations in gyrase/topoisomerase
-efflux pumps and permeability barriers

A

fluoroquinolones

106
Q

peptide chain transfer blocked

A

oxazolidinoes -> ribosomal inhibitor

107
Q

block trnas from A site on 30S subunit

A

tetracyclines -> ribosomal inhibitor

108
Q

induce codon misreading at site A

A

aminoglycosides -> ribosomal inhibitor

109
Q

peptide exit tunnel/translocation blocked

A

macrolides + lincosamides -> ribosomal inhibitor

110
Q

resistance:
-aminoglycoside-modifying enzymes
-mutations in ribosomal rRNA
-mod of ribosome by methyltransferases (its a hat!)
-decrease membrane permeability

A

ribosomal inhibitor

111
Q

helpful for stopping toxin production e.g. staphylocoocal toxic shock syndrome + necrotizing soft tissue

A

ribosomal inhibitor

112
Q

-prodrug enters cell + anaerobic environment promotes reduction to nitroso intermediate products
-these products cause DNA to break

A

mitroimizadoles/metroindazole

113
Q

-intra-abdominal infections
-bacterial vaginosis
-brain abscess

A

mitroimizadoles/metroindazole

114
Q

-inhibits rna polymerase
-combo therapy
-penetrates osteoblasts
-DIFFUSES WELL INTO BIOFILMS

A

rifampin

115
Q

-folate (B9 synthesis)
-important pathway for dna synthesis
-trimethoprim/sulfamethoxazole (SXT) blocks 2 steps in this pathway

A

sulfonamides

116
Q

intrinsic resistance example:
enterococcus can take up folate from the environment as an alt. source= target bypass

A

sulfonamides

117
Q

-disrupt OM of GN
-hydrophillic cationic ring + hydrophobic tail = inserts into membranes
-toxic to kidneys + brain

A

polymyxins

118
Q

not sure what patient is infected with

A

empiric coverage

119
Q

-effectively targets all PBPs
-amp. targets 4 & 5
-ceftriaxone targets 2 & #

A

dual beta-lactam therapy (enterococcus)

120
Q

aminoglycoside + cell wall inhibitor

A

dual therapy (enterococcus)

MICRO 442 (25 decks)

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