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Immunology > Introduction to Infectious Agents 4 > Flashcards

Introduction to Infectious Agents 4 Flashcards

1
Q

bacteria that have cell wall and can’t be used with gram pos/neg stain, what stain can be used?

A

acid-fast stain

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2
Q

acid-fast will stain what color

A

pink

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3
Q

non acid-fast will stain what

A

violet

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4
Q

how do acid-fast stain work

A

bacteria on slide. initial stain: carbol fuchsin. if they take up the carbol fuchsin they will not be decoloriazed with decoloriser. then use counterstain.

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5
Q

what bacteria is acid-fast stain used for

A

mycobacterium

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6
Q

why are mycobacterium cannot do gram stain

A

high wax content in wall

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7
Q

example of acid-fast bacteria:

A

Mycobacterium

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8
Q

what is present in acid fast cell wall

A

Mycolic acid*
Trehalose dimycolate
Lipoarabinomannan
Arabinogalactan

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9
Q

example of bacteria without cell wall

A

mycoplasma

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10
Q

what do bacteria of no cell wall bacteria contain

A

sterols

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11
Q

what do no cell wall bacteria use to maintain fluiditiy

A

sterols

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12
Q

what is function of adhesins on cell wall less bacteria

A

adhesins - allow them to move like caterpillar

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13
Q

where is site of atp production in bacteria

A

plasma/cell memrane

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14
Q

what is plasma/cell membrane made out of in bacteria

A

phospholipid bilyaer

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15
Q

flagella are made of what

A

flagellin proteins

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16
Q

peritrichous

A

flagella all over the surface

“bad hair day”

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17
Q

lophotrichous

A

a tuft of flagella at one end

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18
Q

amphitrichous

A

one or more flagella at each end

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19
Q

monotrichous

A

one flagellum

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20
Q

where is axial filament found

A

only in perplasmic space

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21
Q

pilus and fimbria are made of what

A

pilins (pilus) and fimbrins (fimbria)

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22
Q

what is function of pilus and fimbria

A

adhesion to host cell surface
virulence factor
cell communication

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23
Q

genetic exchange of bacteria - what is needed for this to occur

A

sex pili (F pili)

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24
Q

describe structure of fimbriae on gram neg and gra positive

A

Gram +ve differs from Gram –ve fimbriae

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25
Q

capsule also called

A

glycocalyx and slime layer

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26
Q

what is function of capsule

A

anti-phagocytic (prevents phagocytocsis)
prevent dehydration
antibiotic penetration (makes it hard to treat with antibiotics)

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27
Q

capsules grow around

A

individual bacteria

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28
Q

what grows around colony of bacteria

A

biofilm

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29
Q

biofilm provides what advantage

A

protects against
phagocytosis
dehydration
antibiotic penetration

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30
Q

when is biofilm a huge bad thing in medical

A

if they grow on implanted stuff in body

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31
Q

what is genetic material in bacteria

A

hapoid DNA chromosome wound in nucleoid

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32
Q

pathogenicity islands

A

tend to find aggregation of genes that have antibiotic resistance, etc.
have G+C content

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33
Q

plasmids

A

extra chromosomal genetic elements

non-essential genetic info

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34
Q

what is an example of what can be contained in a plasmid

A

drug resistance

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35
Q

how many copies of plasmid

A

one or more ( no more than 20)

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36
Q

ribosomes in bacteria

A

70S

require N-formyl

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37
Q

what is significant about N-formyl on ribisomes in bacteria

A

chemoattractants - we have receptors that can recognize and bind to them and destroy. esp. neutrophils

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38
Q

in storage granules in bacteria what will be depsotied

A

glycogen
lipids
polyphosphates

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39
Q

why are storage granules used in bacteria

A

when ther eare unfavorable conditions

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40
Q

endospores

A

not reproductive - theya re just formed to allow bacteria to survive unfavorable conidions
not metabolically active

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41
Q

what does the core of endospore contain

A

high concentrations of calcium bound to dipicolini acid + keratin-like protein

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42
Q

draw a endospore

A

pg 50

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43
Q

within dehydrated core what will you find in endospores

A

ribosomes

44
Q

what are 3 main wais bacteria uptake material

A

facilitated diffusion
active transport
group trnaslocation

45
Q

can facilitated difussion work against concentration gradient

A

no

46
Q

can active transpot and group translcoation work against concentration gradient

A

yes

47
Q

group translocation

A

material that is translocated is modified by chemical group, usually phsphate from pyruvate. it is similar to active transport except that it is modified.

48
Q

in gram neg. bacteria how many secretion systems are there

A

6

49
Q

type III secretion apparatus in gram neg. is used to do what

A

used to inject toxins into host cell

50
Q

what is type III secretion apparatus similar to in function

A

syringe

51
Q

bacterial products (name 3)

A

exoenzymes
exotoxins
endotoxins

52
Q

endotoxins

A

endotoxins not released but can be following bacterial cell damage

53
Q

exoenzymes

A

degradative/hydrolytic

ex: lipases, proteases, hyaluronidase, hemolysins, DNases

54
Q

certain species of bacteria secrete enzyme that forms clot, and what does clot do

A

surrounds bacteria

55
Q

exotoxins - three main clases

A

A-B toxins
membrane-disrupting toxins
superantigens

56
Q

exotoxins

A

produced by gram pos and gram neg.
never secreted through type III secretion appartus
have ot bind to receptor on surface of host cell to get into cell

57
Q

A-B toxins what are subuntis

A

A & B

58
Q

b subunit does what

A

binds to receptor on surface of cell

59
Q

ex of b subunit

A

cholera toxin

60
Q

A subunit does what

A

activates adenylyl cyclase which leads to disuprtion (in cholera)
mediates enzymatic activity resopsneible for toxcitiy

61
Q

vaccines against A-B toxins

A

go against B subunit to prevent it from biding, it prevents toxin activity

62
Q

what are two main ways that membrane disrupting toxins work

A

pore (channel) former

destruction of phospholipid bilayer (lipase activity)

63
Q

superantigens

A

stimulate 20-25% of T cells

- superantigen binds to T cell receptor and APC - binds to ones that have particular V gene segments

64
Q

normal way T cells recognize antigen

A

MHC class II presneting to receptor of T cell - T cell receptor recognizes peptide bound

65
Q

what is result of superantigens

A

activates a lot of T cells but they are not specific

66
Q

what can high levels of T cells being activated to

A

high levels of cyokines - toxic shock (cytokine storm)

67
Q

what is result of endotoxic shock

A

bulk movement of fluid from circulation into tissues

68
Q

endotoxic shock

A

collapse of blood vessels - leads to disseminated intravascular coagulation - death of cells and tissue b/c of hypoxic damage

69
Q

what does DIC stand for

A

disseminated intravascular coagulation

70
Q

bactericidal drug used if it is gram neg what happens

A

LPS release if it is gram negative

71
Q

endotoxins are all

A

polysaccharides

72
Q

exotoins are

A

protein

73
Q

endotoxin and exotoxin are both

A

antigenic

74
Q

endotoxin relationship to cell

A

part of outer membrane

75
Q

exotoxin relationship to cell

A

extracellular, diffusible

76
Q

can endotoxin and exotoxin form toxoid?

A

endotoxin - no

exotoxin - yes (vaccine)

77
Q

special stains can be used to detect what

A

spores, capsule, falgellla

78
Q

lot of method for identifying bacteria involves what

A

culture

79
Q

selective media

A

allows growth of some species but not others

80
Q

selective media

A

allows growth of some species but not others

81
Q

list some common methods to diagnose bacterial infection

A

pg 62

82
Q

what does serology tell you

A

if person was affected, can’t tell you if person is currently affected.
only way you can say currently is if you see increase in antibiotics over certain time

83
Q

what do you use for molecular analyses for diagnosis of bacteria

A 
PCR amplification
DNA probes (in situ hybridization)
84
Q

what is direct way to measure bacterial growth

A

microscopy

85
Q

what is indirect way to measure bacteria growth

A

plate (CFU)

86
Q

why is indirect more affective than direct (microscopy vs. plate)

A

on plate you are seeing live bacteria. microscopy can’t distinguish

87
Q

describe growth curve of bacterial growth

A

lag
exponential
stationary
death

88
Q

describe growth curve of bacterial growth

A

lag
exponential
stationary
death

89
Q

under optimal conditions what is generation time of E. Coli

A

15-20 minutes

90
Q

the bacteria that causes gangrene is what kind of bacteria

A

anaerobe

91
Q

what do you do with deep wound with gangrene setting in and why

A

open wound to let oxygen in - kills the clostridia bacteria

92
Q

what are rapid screening assays available now called

A

biotyping

93
Q

how does biotyping work

A

substrates that some bacteria use and some can’t use

substrates chosen so if bacteria can use them there will be colored change on strip

94
Q

What makes up the thick peptidoglycan layer in the cell wall of both gram pos. and gram neg. bacteria?

A

N-acetyl muramic acid

N-acetyl glucosamine

95
Q

What does NAM stand for

A

N-acetyl muramic acid

96
Q

What does NAG stand for

A

N-acetyl glucosamine

97
Q

what will be found in gram pos but not in gram neg in peptidoglycan layer

A

Teichoic acids

Lipoteichoic acids

98
Q

exoenzymes are generally:

A

degradative enzymes

99
Q

name some example exoenzymes

A 
lipases
proteases
hyaluronidase
hemolysins
DNases
100
Q

describe how bacteria can penetrate to subepithelial layer of host

A

secrete exo-enzymes that break down basement membrane

101
Q

describe how bacteria can secrete a clot and use it to their advantage

A

they secrete enzyme that secretes a clot so the body’s immune system can’t get to the bacteria. the clot surrounds bacteria. then they secrete enzyme that initiates disassembly of the clot and bacteria can go about their business

102
Q

high level of LPS (in cell wall of gram neg. bacteria) what happens?

A

high production of cytokines → can result in endotoxic shock
causes bulk movement of fluid from circulation into tissues → hypotension → collapse of blood vessels → activation of coagulation cascade → lots of coagulation in lumen of blood vessels → occludes blood tissues → hypoxic death

103
Q

What does DIC stand for

A

disseminated intravascular coagulation

104
Q

why is there DIC in endotoxic shock?

A

widespread release of LPS

105
Q

bactericidal vs. bacteriostatic drug

A

bactericidal drug and have high level infection w/ gram neg bacteria will cause widepread release of high levels of LPS
sometimes just better to use bacteriostatic drug and leg immune system kick in

106
Q

what is the name of the bacteria that causes gangrene

A

clostridia

Immunology (12 decks)

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