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Winter 2016 > D&D Unit 4 > Flashcards

D&D Unit 4 Flashcards

1
Q

What are the 3 cytoskeletal elements in bacteria we care about? What do they do?

A

FtsZ - division. Tubulin-like.
MreB - shape, polarity, chromosome segregation. Actin-like
CreS - shape. Intermediate filament-like

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2
Q

Peptidoglycan is composed of which 2 sugars?

A

N-acetylglucosamine

N-acetylmuramic acid

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3
Q

How does the amount of cross-linking in peptidoglycan chains vary between gram-positive and negative bacteria?

A

It is much greater in gram-positive bacteria

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4
Q

Which enzyme made by the body hydrolyzes peptidoglycan?

A

Lysozyme - it cleaves the glycosidic bond between the 2 sugar types

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5
Q

What extra 2 components does the gram-positive cell surface have compared to the gram-negative cell surface?

A

Teichoic acid

Lipoteichoic acid

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6
Q

What extra 3 components does the gram-negative cell surface have compared to the gram-positive cell surface?

A

Lipopolysaccharides
Lipoproteins
Porins

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7
Q

What 2 important antigens does the lipopolysaccharide of gram-negative bacteria contain?

A

Lipid A - toxic part of endotoxin
O antigen - side chain oligosaccharides

In the middle is the core polysaccharide

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8
Q

What is techoic acid made of?

A

Repeating polyglycerol-P or polyribitol-P

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9
Q

What makes up biofilms?

A

Extracellular glycocalyx

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10
Q

What is it calle when bacteria have flagella distributed over their surface? At one end?

A

Peritrichous

Polar

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11
Q

Where is the bacterial DNA located?

A

Nucleoid (a region of cytoplasm)

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12
Q

____________ is when a bacteria’s gene expression and thus phenotype is changed because of infection with a bacteriophage

A

Phage conversion

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13
Q

What are the 4 stages of the bacteria growth curve?

A
  1. Lag phase - period of physiologic adjustment for the starting cells
  2. Exponential phase - rate of increase in cells is proportional to the number already present
  3. Stationary phase - nutrients are consumed and toxic metabolic byproducts accumulate
  4. Death (only sometimes occurs)
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14
Q

What is a microaerophilic bacterium?

A

It grows best at low oxygen concentrations though it can grow without oxygen

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15
Q

What is sporulation?

A

A response to nutrient-limited conditions. Bacteria differentiate to form highly resistant, dehydrated forms that have no metabolic activity.

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16
Q

Antimicrobial agents work on the principle of ___________

A

Selective toxicity - selective inhibition of microbial growth at drug concentrations colerated by the host

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17
Q

What is a selective medium for growing bacteria?

A

One that allows for visible differentiation of organisms

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18
Q

What is an enrichment medium for growing bacteria?

A

One that allows a particular one to grow more than others

In contrast to a selective medium that suppresses the growth of some bacteria

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19
Q

A plasmid the confers resistance to an antimicrobial is an _________

A

R factor

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20
Q

What are insertion sequences?

A

Transposons that encode transposase

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21
Q

What are complex transposons?

A

Ones that encode transposase and additional genes

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22
Q

What are pathogenecity islands?

A

Large segments of bacterial genomes that encode genes that contribute to virulence

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23
Q

What is the major cytotoxic agent released by staph aureus?

A

Alpha-toxin

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24
Q

How does staph aureus reduce phagocytosis?

A

Coagulase enzyme induces fibrin deposition

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25
Q

What is the primary virulence factor in strep throat? What 2 things does it do?

A

M-protein

Inhibits phagocytosis/killing by PMNs
Enhances adherence to epithelial cells

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26
Q

What is the difference between tetanus and botulism toxin?

A

Spastic vs. flaccid paralysis

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27
Q

Most cystic fibrosis patients are chronically infected with ___________ by age 15-20

A

Pseudomonas aeruginosa

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28
Q

What part of Neisseria gonorrhea is required for virulence?

A

Pilus

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29
Q

What is trachoma?

A

Chlamydia infection of the eye

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30
Q

Where does staph aureus normally hang out?

A

Anterior nares

Perineum

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31
Q

The lupus anticoagulant is what?

A

IgG against phospholipid

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32
Q

_____________ is the major constituent of fungal membranes vs. _____________ in mammalian membranes

A

Ergosterol

Cholesterol

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33
Q

What is the difference between a bactericidal vs. a bacteriostatic agent?

A

Bactericidal - organisms are killed via inhibition of cell wall synthesis, disruption of cell membrane funciton, interference with DNA function or synthesis

Bacteriostatic - organisms are prevented from growing by inhibition of protein synthesis (except animnoglycosides, which are bactericidal), intermediary metabolic pathways

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34
Q

Whdn do you take antibiotics on an empty stomach? When do you take it with food?

A

Empty stomach - when a higher pH is needed

Food - when the drug is acid stable but may irritate stomach

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35
Q

What are the 3 stages of peptidoglycan formation?

A
  1. Synthesis and assembly of cell wall subunits
  2. Linear polymerizaiton of subunits at cell membrane
  3. Cross-linking of peptidoglycan polymers occurring at cell wall
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36
Q

Beta-lactams acetylate _____________

A

penicillin binding proteins

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37
Q

What bacterial enzyme confers resistance to beta-lactams

A

Beta-lactamase

Hydrolyzes them - splits the amide bond of the ring

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38
Q

What does diptheria toxin do?

A

An ADP ribosyltransferase that inactivates elongation factor 2 (required for peptide chain elongation)

1 toxin molecule per eukaryotic cell

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39
Q

What does pseudomonas aeroginosa exotoxin A (PAE) do?

A

An ADP ribosyltransferase that inactivates elongation factor 2

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40
Q

What 2 bacteria make shiga toxin?

A

Shigella dysenteriae

E. Coli

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41
Q

What does shiga toxin do?

A

An RNA N-glycosidase that inactivates ribosomes

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42
Q

What does staphylococcus aureus look like microscopically?

A

Grapes!

Gram-positive cocci in clusters

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43
Q

Staph alpha-toxin forms a _____________

A

Heptameric pore

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44
Q

What 3 things made by staph contribute fo impaired phagocytosis?

A

Coagulase
Fibrinogen-binding protein
Protein A

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45
Q

What 3 cytokines are most excessively produced in the cytokine storm?

A

IL-2
IFN-Y
TNF-A

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46
Q

Is staph catalase negative/positive? Strep?

A 
Staph = +
Strep = -
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47
Q

Which bacteria causes scarlet fever?

A

Strep

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48
Q

Which bacteria causes rheumatic fever?

A

Strep

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49
Q

How does M-protein reduce phagocytosis?

A

Binds factor H, which reduces C3b on cell surface

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50
Q

3 most common organisms that cause rheumatic fever

A

Staphylococcus aureus
Viridans Streptococci
Coagulase-negative Staphylococci

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51
Q

Which bacteria can we make a vaccine against?

A

Pneumococcus

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52
Q

Do bacterial spores have detectable metabolism?

A

No

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53
Q

Do bacterial genomes have introns?

A

Usually not

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54
Q

What are conjugative and non-conjugative plasmids?

A

Conjugative plasmids promote sexual conjugation between cells

Non-conjugative plasmids can’t initiate conjugation, so they need assistance of conjugative plasmids to transfer

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55
Q

4 steps needed to demonstrate that a toxin participates in the pathogenesis of an infectious disease

A
  1. purified toxin produces characteristic signs/symptoms of infectious disease
  2. Administration of antitoxin prevents development of the disease if the infectious agent is given
  3. Virulence of infectious agent reflects the amount of toxin it produces (somewhat questionable)
  4. Strains lacking ability to produce toxin are decreased in virulence or are avirulent
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56
Q

Which types of bacteria make endotoxin?

A

Gram-negative bacteria

They shed pieces of lipipolysaccharides

57
Q

What are superantigens?

A

Microbial exotoxins that corrupt mechanisms of immunity

They trigger excessive and abberant activation of T-cells

58
Q

What are the 2 subunits of diptheria toxin?

A

B-subunit is for cell entry (not all cells have the receptor)

A-subunit is the part that catalyzes transfer of ADP-ribose part of NAD onto EF-2 in the cytoplasm. The EF-2 can’t function in protein synthesis

59
Q

What is the primary treatment for diphtheria?

A

Antitoxin

Antibiotics are used to prevent spread

60
Q

Are diptheria toxin and exotoxin A (pseudomonas aeruginosa) the same?

A

NO they have no homology

Different cell receptors, cell types, amino acid sequences

61
Q

What is type III toxin secretion?

A

Toxins are injected directly into eukaryotic cells

Many gram- bacteria can do this

62
Q

What is type IV toxin secretion?

A

Injection of toxin (and nucleic acids too) by conjugation-like bacterial machinery

63
Q

Which type of bacteria has an outer membrane?

A

Gram -

64
Q

What type of stuff do porins allow to pass through the outer membrane of gram- bacteria?

A

Hydrophilic stuff

65
Q

What enzymes cross-link peptidoglycan?

A

Penicillin binding proteins

66
Q

What does the peptidoglycan precursor have that antibiotics can target?

A

D-alanine-D-alanine

It is cleaved off during cross-linking

67
Q

Carbapenemases are __________-mediated

A

Plasmid

68
Q

Whatgene confers resistance in MRSA?

A

mecA

PBP2a - A low affinity penicillin-binding protein

Confers resistance to all beta-lactam agents

Only in staph

69
Q

What are mosaic PBPs?

A

Mostly in strep pneumoniae and Neisseria gonorrhoeae

They can pick up pieces of genetic material from other bacteria and swap them with similar pieces of DNA of their own

70
Q

What are the 2 places superantigens (made by bacteria) bind?

A 
MHC class II
Vd chains on T cells

Thus, they activate much larger numbers of T cells than any specific antigen does

71
Q

What are the 3 ways bacteria can get new genetic material?

A

Conjugation - bacteria

Transduction - virus (that took the genes from another bacteria)

Transformation - environment

72
Q

What are the heat-labile enterotoxins of Vibrio cholera and E. coli?

A

ADP ribosyltransferases that cause active chloride secretion leading to secretory diarrhea

73
Q

Which 2 bacteria cause secretory diarrhea caused by chloride secretion?

A

Vibrio cholera

E. coli

74
Q

Which 5 bacteria make ADP ribosyltransferase toxins?

A

Inactivation of EF-2: diptheria, pseudomonas aeruginosa (the toxins are different though!)

Secretory diarrhea - Heat-labile enterotoxins of Vibrio cholera and E. coli

Pertussis

75
Q

What are the gram+ cocci we care about? 2 (2,4)

A

Staph: Aureus, SSNA (staph specia, not aureus)

Strep: Pyogenes, pneumoniae, ‘viridans’, Enterococcus faecalis, Enterococcus faecium

76
Q

Which bacteria causes toxic shock syndrome?

A

Staph

77
Q

Which bacteria makes slime and adheres to foreign bodies like implants?

A

Staph epidermidis

SSNA/CNS (staph species, not aureus/coagulase-negative staph)

78
Q

What does strep pneumoniae look like under the microscope?

A

Gram positive

Pairs

79
Q

3 bactericidal mechanisms

A

Inhibition of cell wall synthesis
Disruption of cell membrane function
Interference with DNA function/synthesis

80
Q

2 bacteriostatic mechanisms

A

Inhibition of protein synthesis (except amnoglycosides, which are bactericidal)
Inhibition of intermediary metabolic pthways

81
Q

What is the rule of thumb for determining which antibiotics can cross the placenta?

A

The ones taken orally usually can

82
Q 
Where do the following antibiotics distribute?
Clindamycin
Macrolides
Tetracyclines
Nitrofurantoin
Aminoglycosides
A

Clindamycin - bone
Macrolides - pulmonary cells
Tetracyclines - gingival crevicular fluid, sebum. Also developing bone and teeth.
Nitrofurantoin - urine
Eminoglycosides - inner ear and renal brush border

83
Q

What 2 things do we use to monitor renal status?

A

Seum creatinine

Creatinine clearance

84
Q

The persistent suppression of bacterial growth that may occur after limited exposure to some antibacterial drugs is called ____________

A

Post antibiotic effect

85
Q

What are 2 gram negative rods we care about?

A

E. coli

Pseudomonas aeroginosa

86
Q

What is the gram positive rod anaerobe we care about? The gram negative rod anaerobe?

A

Clostridium difficile

Bacteroides fragilis

87
Q

What is the distribution for penicillins?

A

They are ionized at physiological pH so they mostly enter inflamed tissues

88
Q

How are penicillins excreted?

A

Mostly excreted as an active drug via the kidney (remember that they used to reuse penicillin from people’s urine)

89
Q

How is vancomycin administered?

A

IV (unless it’s for stuff in the GI tract like C. difficile)

90
Q

Which 2 bacterial groups is vancomycin used for?

A

Gram positive cocci: staph and strep

Anaerobes: C. difficile

91
Q

What does the heat-stable enterotoxin of E. coli di?

A

Increase cellular cGMP, leading to secretory diarrhea

92
Q

What are the 3 main toxins E. coli produces?

A

Shiga
Heat-labile enterotoxin
Heat-stable enterotoxin

93
Q

What toxin does Bacillus anthracis produce?

A

Anthrax edema factor

94
Q

What is intrinsic drug resistance?

A

MIcrobes lack a target for drug action

95
Q

What are 2 advantages to bactericidal agents?

A

Act more quickly and irreversibly (sustained effect)

96
Q

Macrolides (MAC) are effective against:

A

MRSA
Atypical bacteria
the Clap

97
Q

What are the narrow spectrum-prototype penicillins?

A

Penicillin G - Penicillin V

98
Q

Which penicillin is penicillinaseresistant

A

Dicloxacillin

99
Q

Which 3 penicillin drugs that are extended spectrum?

A

They have increased hydrophilicity so they can get through the pores of gram-negative bacteria

Amoxicillin
Ampicillin
Piperacillin

100
Q

Which penicillin is anti-pseudomonal?

A

Piperacillin

101
Q

What are 2 drugs that can be added in order to inhibit beta-lactamases?

A

Clavulanic acid + amoxicillin or ticarcillin

Tazobactam + piperacillin

102
Q

What is the sufix for macrolides?

A

-mycin

Erythromycin
Clarithromycin
Azithromycin

103
Q

What are 2 tetracyclines?

A

Tetracycline

Docycycline

104
Q

What is the suffix for fluoroquinolones?

A

-Floxacin
Ciprofloxacin
Levofloxacin
Moxifloxacin

105
Q

What does staph aureus do on a blood agar plate?

A

It is beta-heolytic

106
Q

What is the main virulence factor for staph aureus?

A

Protein A

Prevents complement from doing its thing by by binding Fc portion of immunoglobulins

107
Q

Which bacteria usually causes septic arthritis in adults?

A

Staph aureus

108
Q

What antibiotic do you use for MRSA? What about regular staph?

A

Vancomycin

Penicillin - Nafcillin (naph for staph)

109
Q

What is a mean feature of 3rd generation cephalosporins?

A

They can penetrate the CNS

110
Q

What is the definition of minimum inhibitory concentration?

A

The lowest concentration of antibiotic that prevents visible bacterial growth

111
Q

Penicillin is for gram-_________ infections

A

Positive

112
Q

Cephalosporins have the prefix _________

A

cef-

113
Q

Absorption of oral tetracyclines is impaired by _________

A

Milk

114
Q

The clostridium genus is gram_________, what sort of metabolism, and does or does not form spores?

A

Positive
Obligate anaerobes
Forms spores

115
Q

What does the AmpC gene do?

A

Beta-lactamases that are cephalosporinases

It is inducibly expressed

116
Q

Why don’t penicillins or ampicillins work against staph anymore?

A

Most contain the bla (beta-lactamase) plasmid

117
Q

What is antiobiotic tolerance/escape?

A

Bacteria are susceptible to antibiotics but the antibiotics don’t work

Usually because of some metabolic resistance

118
Q

Which group of bacteria is intrinsically resistant to vancomycin?

A

Gram-negative rods

119
Q

What does a positive D-test indicate?

A

Resistance to clindamycin induced by macrolides

120
Q

What is endotoxin?

A

Lipid A, which is part of the lipopolysaccharide of gram- bacteria

121
Q

2 post-streptococcal diseases

A

Glomerulonephritis - type III hypersensitivity

Rheumatic fever - type II hypersensitivity

122
Q

What is the pneumonia vaccine for?

A

Streptococcus pneumoniae

123
Q

What bacteria makes alpha toxin?

A

Clostridium perfringens

124
Q

What 2 properties of E. coli are essential for GI disease?

A

Adherence to the intestinal mucosa via pili

Toxins that disrupt the electrolyte balance in teh gut

125
Q

E. coli UTI strains are _____________-hemolytic

A

Beta

126
Q

What do we use to treat pseudomonas?

A

Piperacillin + tazobactam (piper suitor)

Aminoglycoside and fluoroquinolones

127
Q

What class of bacteria do penicillins work best against?

A

Gram positive cocci - purple round ships in Princess Ellen’s New Hope

S. Pneumoniae
S. Pyogenes
Enterococcus

NOT MSSA or MRSA

128
Q

How are penicillins V and G taken?

A

V is oral because it is acid stable (oral in Princess Ellen’s New Hope)

G is IV (ivy trapping Princess Ellen)

129
Q

Where does bacteroides live?

A

In the gut

130
Q

What are the 2 E coli enterotoxins?

A

Heat-stable - cAMP

Heat-labile - cGMP

131
Q

What toxin does pertussis produce? What does it require?

A

Adenylate cyclase toxin

Requires activation by calmodulin and calcium

132
Q

What does anthrax lethal factor do?

A

It is an endopeptidase that cleaves MAPKK proteins and fucks shit up!

133
Q

What are the 2 C diff toxins?

A

They are glucosyl transferases
A - attracts neutrophils
B - alters actin

134
Q

Tetanus and botulinum toxins are ________-dependent endopeptidases that inactivate _________, preventing ___________

A

Zinc
SNARE
Neuroexocytosis

135
Q

What are the 2 parts of an toxin with intracellular targets?

A

A - active

B - binding

136
Q

How are beta lactamases conferred?

A

Plasmids

137
Q

How is amoxicillin administered? How is ampicillin administered?

A

Oral - Han Cillin is eating

IV - ivy guitar cord

138
Q

What confers resistance to aminoglycosides?

A

Acetyl-phospho-adenylyl transferase

Enterococci

Enterococci drummer throwing ninja stars

139
Q

What confers resistance to chloramphenicol?

A

Acetyltransferase

Staph, streph, Neisseria

Winter 2016 (8 decks)

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