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immunology & pathogenesis > Final > Flashcards

Final Flashcards

1
Q

How does a capsule protect a pathogen?

A
  • Prevents PAMP-PRR interactions
  • if it has sialic acid it can bind to serum protein H and degrade opsonin C3b
  • some prevent formation of C3 convertase
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2
Q

Capsules with silica acid do what?

A

bind to serum protein H which leads to degradation of opsonin C3b

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3
Q

How does the host fight a capsule?

A

produce opsonizing antibodies specifically against the capsule

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4
Q

Streptococcus progenies evades complement how?

A

M protein binds serum factor H which degrades C3b

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5
Q

How do pathogens get around antimicrobial peptides?

A
  • charge repulsion
  • peptidases
  • reduced uptake of peptides because of capsule
  • efflux pumps
  • biofilm
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6
Q

virulence factors enable bacteria to do what?

A
  • attach and colonize
  • invade and disseminate
  • evade host immune system
  • eat and grow
  • spread
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7
Q

How can you evade the adaptive immune system?

A
  • antigenic variation
  • molecular mimicry
  • IgA proteases
  • protein A, protein G
  • biofilm
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8
Q

How does Neisseria use antigenic variation to escape antibodies?

A

pili as adhesins and different subsets of pili

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9
Q

How do flu viruses use antigenic variation to escape antibodies?

A
  • mutations and seasonal variations of flu strains
  • antigenic drift
  • antigenic shift
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10
Q

molecularly mimicry example

A

streptococcus capsule is made of hyaluronic acid which is commonly found in the body

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11
Q

Which proteins does streptococcus produce?

A

proteins A and G

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12
Q

What do proteins A and G do?

A

bind to Fc region of antibodies (instead of epitopes)

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13
Q

How can pathogens avoid cytotoxic T cells?

A
  • kill them
  • interfer with MHC
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14
Q

pseudomonas classification

A
  • aerobic
  • Gram -
  • metabolically diverse
  • saprophytes (feed on decaying organisms)
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15
Q

is pseudomonas motile?

A

yes it has polar flagella

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16
Q

Why do some strains of pseudomonas appear mucoid?

A

polysaccharide alginate

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17
Q

what does pseudomonas smell like?

A

grapey

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18
Q

what color is pseudomonas and why?

A

blue green pigment pyocyanin

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19
Q

p aeruginosa is what type of infection?

A

opportunistic and often nosocomial

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20
Q

How does p aeruginosa spread?

A

environment (NOT patient to patient)

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21
Q

How does p aeruginosa attach?

A

pilus and non-plus adhesins

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22
Q

What type of motility does p aeruginosa have?

A
  • swimming
  • swarming
  • twitching
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23
Q

What enzymes does p aeruginosa make?

A
  • toxins
  • proteases
  • DNAases
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24
Q

what type of pili does p aeruginosa use to attach to host cells?

A

type 4

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25
Q

What type of toxins does p aeruginosa secrete?

A

type 3

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26
Q

What does staphylococcus aureus look like?

A

a bunch of golden grapes

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27
Q

Staphylococcus classification

A
  • gram +
  • non-motile
  • non-spore forming
  • facultative anaerobe
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28
Q

staphylococcus aureus is what type of pathogen?

A

commensal and nosocomial

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29
Q

How does MRSA do?

A

change penicillin binding protein (PBP)

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30
Q

How do vancomycin do?

A

inhibits cell wall synthesis by binding to hanging chain of peptidoglycan

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31
Q

How do VRSA do?

A

modify binding site and replace with low-affinity precursors

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32
Q

what are the staphylococcus aureus adhesins

A

fibrinogen, fibronectin binding surface proteins Fnbp A and B, ClfA and B, IsdA, and WTA

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33
Q

how does staphylococcus aureus inhibit phagocytosis

A
  • capsule
  • proteins A and G which bind to Fc region of IgG antibodies and avoid opsonization
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34
Q

how does staphylococcus aureus inhibit neutrophil migration

A
  • inhibitory protein (CHIPS) binds to and inhibit chemotactic receptors
    extracellular adherence protein (Eap) decreases ICAM-1 expression on endothelial cells
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35
Q

How does staphylococci aureus inactivate reactive oxygen species?

A
  • golden carotenoid pigment
  • superoxide dismutase (SOD)
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36
Q

how does staphylococcus aureus reduce the activity of antimicrobial peptides?

A

protease aurolysin causes the AMP to hydrolyze

37
Q

how doe staphylococcus aureus alter the adaptive immune response?

A
  • super antigens which activate T cells by cross linking TCR with MHC II molecules
  • this bypasses the requirement for specific TCR recognition of MHC II-peptide complex
38
Q

facultative intracellular pathogens

A
  • listeria
  • mycobacterium
  • salmonella
39
Q

obligate intracellular pathogens

A
  • coxiella
  • chlamydia
40
Q

the phagolysosome contains what?

A
  • reactive oxygen and nitrogen species
  • superoxide anion
  • hydroxyl radical
  • hypochlorite
  • hydrolytic enzymes
  • lysozymes
  • lactoferrin
  • AMPs
  • acidic pH
41
Q

neutrophil extra cellar traps (NETs)

A
  • specific tool that allows neutrophils to capture and effectively destroy a broad range of pathogens while minimizing host damage
  • extracellular fibrous structures composed of decondenses intracellular DNA associated with AMPs such as neutrophil elastase (NE), lactoferrin, MPO, calprotectin, cathepsin G, histones, and some other cytoplasmic proteins
42
Q

How does mycobacterium survive?

A

arrests the maturation of phagolysosome in an easy endosome-like vesicle

43
Q

which bacteria lyse the phagosomal membrane and escape into the cytoplasm?

A

listeria and shigella

44
Q

which bacteria fuses with ER

A

legionella

45
Q

which bacteria directs the maturation of a phagolysosome-like compartment

A

coxiella

46
Q

which bacteria activate acid tolerance gene allowing adaptation to the acidic pH?

A

salmonella

47
Q

mycobacterium tuberculosis classification

A
  • obligate aerobe
  • nonsporulating
  • non motile
  • rods
  • slow growing
48
Q

how to kill mycobacterium tuberculosis

A

reistant to acid, alkali, drying, germicides, antibodies, and complement

49
Q

mycobacterium tuberculosis strategy one to conquer macrophages

A
  • interferons with phagosome functions by inhibiting the phagolysosome biogenesis
  • the vacuole does not mature following the normal endocytic pathway and resembles an immature endosome
  • blocks phagosomal acidification
  • inhibits H+ V-ATPase complex assembly and its subsequent fusion with the phagosomal membrane resulting in the stabilization of the phagosomal pH between 6.2 and 6.5
50
Q

mycobacterium tuberculosis strategy two for conquering a macrophage

A

access the cytosol through ESX-1 secretion system

51
Q

mycobacterium tuberculosis strategy three to conquer a macrophage

A

cytosolic mycobacterium tuberculosis induces host cell death programs to enhance its dissemination

52
Q

which bacteria can disrupt the phagosomal membrane and cause the release of bacterial products, including its own DNA, into the macrophage cytosol

A

mycobacterium tuberculosis

53
Q

which bacteria blocks the assembly of iNOS with phagosomes and resists damage by NO

A

mycobacterium tuberculosis

54
Q

listeria classification

A
  • facultative intracellular anaerobe
  • non-spore forming
  • Gram + rods
  • flagella mediating tumbling motility
55
Q

what the temperatures can listeria grow at

A

1-45C

56
Q

how is a listeria infection initiated

A

infect the M cells in intestinal Peyer’s patches and then spread intracellularly

57
Q

how does listeria avoid being killed?

A
  • delays the maturation of the phagosome
  • destroys the phagosomal membrane and replicates in the cytosol
58
Q

key steps in listeria intracellular survival

A
  • internalization
    • internals A and B mediate uptake, even by non-phagocytic cells
  • phagosomal escape
    • listeriolysin O is a pore forming toxin that facilitates bacterial escape from the phagosome
  • spread from cell to cell
    • ActA polymerizes host actin into tails that propel the bacteria into neighboring cells
59
Q

legionella classification

A
  • facultative intracellular
  • small Gram - rods
60
Q

does legionella do human to human transmission

A

no

61
Q

what bacteria enter the ER lumen and how

A

legionella by altering phagosome transport to send them to the ER and turns the phagosome ER-like

62
Q

coxiella burnetii classification

A
  • weak Gram -
  • obligate intracellular
  • requires acidic pH for replication
63
Q

coxiella burnetii transmission

A

normally from farm animals, not usually human to human

64
Q

LD50 of coxiella burnetii

A

one (one will kill 50% of the test organisms)

65
Q

how does coxiella burnetii do?

A

actively directs the maturation of a phagolysosome-like compartment known as the coxiella containing vacuole or a parasitophorous vacuole

66
Q

coxiella burnetii is phagocytosed through what mechanism

A

actin dependent

67
Q

the coxiella containing vacuole acquired what following internalization

A

RAB5

68
Q

what accumulates in the CCV?

A

cathepsin D

69
Q

what two staphylococcus aureus toxins are superantigens

A
  • TSST-1 - topic shock syndrome toxin
  • SE - staphylococcal enterotoxin
70
Q

staphylococcus aureus exfoliative toxin (ET)

A
  • exoenzyme (a group of proteases)
71
Q

staphylococcus aureus staphylokinasze (Sak)

A
  • exoenzyme that dissolves clots and helps bacteria move through tissue and escape abscesses
72
Q

staphylococcus aureus alpha-toxin

A
  • exotoxin that forms pores in human cell membrane
  • defense against neutrophils and other immune cells
  • implicated in necrotizing pneumonia caused bu CA-MRSA
73
Q

staphylococcus aureus leukocidin

A

kills leukocytes and damages cell membranes

74
Q

how does staphylococcus aureus regulate toxin expression

A
  • quorum sensing
  • Repressor Of Toxins (ROT) - repressor protein that regulates 146 genes (most are toxins)
  • RNAIII molecule interacts with rot mRNA to degrade the repressor and produce the toxins
75
Q

live attenuated vaccine pros

A
  • promotes humoral and cell mediated responses
  • often lifelong immunity
76
Q

live attenuated vaccine cons

A
  • strong reaction
  • may mutate back to pathogenic form
  • may need to be refrigerated
77
Q

how to make live attenuated vaccines

A

culture the strains in different host cells (example monkey) for long periods of time to decrease their virulence

78
Q

faster way to create live attenuated vaccines

A
  • mutate or delete the virulence gene
79
Q

killed vaccines pro

A
  • heat or chemical inactivates so no reversion to pathogenic form
  • more shelf stable generally
80
Q

killed vaccine cons

A
  • often requires boosters
  • doesn’t replicate in the host
81
Q

subunit vaccines

A

only use selected antigens not the whole organism

82
Q

subunit vaccine uses what derived from pathogen

A

purified macromolecules

83
Q

tetanus and diphtheria macromolecules are what

A

inactivated exotoxins/toxoids

84
Q

haemophilus macromolecules are what?

A

capsular polysaccharides

85
Q

Hep B and HPV macromolecules are what?

A

surface glycoproteins or recombinant protein Ag

86
Q

toxoid vaccines (subunit vaccines) creation

A
  • inactivate the exotoxin by chemicals
  • body creates toxin neutralizing antibodies
87
Q

toxoid vaccine pro

A

doesn’t activate cytotoxic T cells

88
Q

toxoid vaccine con

A

requires several boosters (tetanus shot)

89
Q

how do you increase the efficacy of subunit vaccines

A

conjugate certain antibodies to carriers (macromolecules)

immunology & pathogenesis (13 decks)

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