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Spring 2025 Therapeutics V > Exam 1: Intro to ID > Flashcards

Exam 1: Intro to ID Flashcards

1
Q

Which bacteria retain crystal violet and iodine (stain purple): Gram + or Gram -?

A

Gram +

*note that Gram - bacteria are counterstained with safranin dye and appear pink/red

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2
Q

How does the Gram + bacteria’s peptidoglycan cell wall vary from Gram - bacteria?

A

Gram + bacteria: Have a thick peptidoglycan cell wall which is why they retain crystal violet

Gram - bacteria: Have a thin peptidoglycan cell wall

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3
Q

What are atypical bacteria?

A

Bacteria that do not stain using a Gram-stain

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4
Q

What are Acid-Fast Bacilli (AFB)?

A

Bacteria resistant to decolorization procedures by acids/ethanol

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5
Q

What is an example of an Acid-Fast Bacilli (AFB)?

A

Mycobacterium species

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6
Q

Most medically important Gram + pathogens are what type?

A

Cocci

(most bacilli are contaminants/ normal flora)

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7
Q

Which cocci species form clusters?

A

Staphylococcus

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8
Q

Which cocci species form pairs/chains?

A

Streptococci
Enterococci

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9
Q

The catalase test is used to differentiate between which two species?

A

-Staphylococci
-Streptococci

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10
Q

The coagulase test is used to differentiate between which two species?

A

-Staphylococcus aureus

-Coagulase-negative staphylococcus (CoNS)

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11
Q

alpha-hemolytic bacteria appear in which part of the body?

A

Oral flora

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12
Q

beta-hemolytic bacteria appear in which part of the body?

A

Skin, Pharynx, Genitourinary

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13
Q

gamma-hemolytic bacteria appear in which part of the body?

A

Gastrointestinal

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14
Q

What are the HACEK organisms?

A

-Haemophilus
-Actinobacillus
-Cardiobacterium
-Elkenella
-Kingella

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15
Q

Most Gram (-) pathogens are what?

A

Bacilli

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16
Q

Lactose fermentation is used to identify which two Gram (-) groups?

A

-Enterobacterales (enteric gram-negative rods or lactose fermenting gram-negative rods)

-Non-fermenting gram-negative rods

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17
Q

The oxidase test is used to distinguish which two Gram (-) groups?

A

Enteric lactose fermenters

Non-enteric lactose fermenters

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18
Q

What are fastidious organisms?

A

Slow growers
-require special supplement media

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19
Q

Review:

A

Lecture 2 Slide 18 for normal flora

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20
Q

What are Penicillin-Binding Proteins (PBP’s)?

A

Enzymes vital for cell wall synthesis, cell shape, and structural integrity

*beta lactams bind here

*largest drug target

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21
Q

What are 3 examples of Penicillin-Binding Proteins (PBP’s)?

A

Transpeptidases
Carboxypeptidases
Endopeptidases

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22
Q

Binding to which segments of Penicillin-Binding Proteins (PBPs) result in a bactericidal effect?

A

1A
1B
2
3

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23
Q

What is the specific job of the most important Penicillin-Binding Proteins: Transpeptidases?

A

Catalyze the final cross linking in the peptidoglycan structure

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24
Q

What is the cytoplasmic membrane?

A

Acts as a selective barrier

-certain drugs must pass through to reach their target site

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25
Q

What is the Peptidoglycan Layer (Cell Wall)?

A

Permeability barrier for large molecules

*PBPs: proteins essential for cell-wall synthesis

*G(+): thick
*G(-): thin

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26
Q

What is the Outer Membrane composed of (gram-negative bacteria only)?

A

Lipopolysaccharides (LPS): mediate immune response and sepsis

Porins: hydrophilic channels that permit diffusion of essential nutrients and small hydrophilic molecules

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27
Q

What is the Periplasmic Space?

A

Gram (+): Compartment between the cell membrane and cell wall

Gram (-): Compartment between the cell membrane and outer membrane

*Vital for bacterial protein secretion, folding, and quality control

*Acts as a reservoir for virulence factors

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28
Q

What is intrinsic resistance?

A

A bug is always resistant to a given antibiotic

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29
Q

What is acquired resistance?

A

A bug is initially susceptible to a given antibiotic, but develops resistance due to some mechanism

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30
Q

What are the possible mechanisms of Intrinsic resistance?

A

-Absence of target site

-Bacterial cell impermeability

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31
Q

What are the possible mechanisms of Acquired resistance?

A

-Mutation in bacterial DNA (spontaneously vs selective pressure)

-Acquisition of new DNA [chromosomal or extrachromosomal [plasmid])

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32
Q

What are examples of Intrinsic Resistance?

A

Cephalosporins vs Enterococci

B-lactams vs Mycoplasma

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33
Q

What are examples of Acquired Resistance?

A

-Stable derepression of AmpC

-Acquisition of KPC gene in GNRs

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34
Q

What are the 3 genetic elements involved in acquired resistance?

A

-Plasmid
-Transposons
-Phages

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35
Q

What is a plasmid?

A

-Self-replicating, extrachromosomal DNA

**Transferable between organisms

-One plasmid can encode resistance to multiple antibiotics

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36
Q

What are transposons?

A

“jumping genes”

-Genetic elements capable of translocating from one location to another

*Move from plasmid to chromosome or vice versa

-Single transposons may encode multiple resistance determinants

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37
Q

What are phages?

A

Viruses that can transfer DNA from organism to organism

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38
Q

What are the 3 ways that acquired resistance can occur?

A

Conjugation

Transduction

Transformation

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39
Q

What is conjugation?

A

Direct contact or mating via sex pili

-DNA shared via mobile genetic elements (MGE) such as plasmids or transposons

Most common

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40
Q

What is transduction?

A

Transfer of genes between bacteria by bacteriophage (viruses)

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41
Q

What is transformation?

A

Transfer or uptake of “free floating” DNA from the environment

-DNA is integrated into host DNA

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42
Q

Which of the following describes the difference between Gram-positive and Gram
negative bacteria?

a) Gram-positive have a thin cell wall; Gram-negative have a thick cell wall
b) Gram-positive have a thick cell wall; Gram-negative have a thin cell wall
c) Gram-positive have porin channels; Gram-negative lack porin channels
d) Gram-positive have PBP; Gram-negative lack PBPs

A

B) Gram-positive have a thick cell wall, Gram-negative have a thin cell wall

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43
Q

What are the 4 mechanisms of antibiotic resistance?

A

Efflux pumps (pump it out)

Drug inactivating enzyme (chew it up)

Modified drug target (change it up)

Altered cell wall protein/decreased porin production (do not let it in)

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44
Q

What is a B-lactamase?

A

An enzyme that hydrolyzes the beta-lactam ring by splitting the amide bond

*Inactivates drugs

*These are produced by bacteria as a resistance mechanism against beta-lactam antibiotics

*beta-lactam antibiotics are the largest and safest drug class so we do not want resistance to occur against these

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45
Q

What are the 2 ways that B-lactamases can be classified?

A

Ambler class: classified according to amino-acid structure (Class A-D)

Bush-Jacoby-Medeiros: classified according to functional characteristics

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46
Q

What are the 2 types of B-lactamase?

A

Serine beta-lactamases: serine residue at the active site

Metallo-beta-lactamases (MBL): zinc residue at the active site

*see lecture 2 slide 31 for picture

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47
Q

What 3 types of B-lactamases are considered Ambler Class A?

A

Narrow-spectrum B-lactamases

Extended-spectrum B-lactamases (ESBL)

Serine carbapenemases

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48
Q

What is the function of Narrow-Spectrum B-lactamases and which bacteria produce them?

A

-Hydrolyze Penicillin

-Produced by Enterobacterales

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49
Q

What is the function of Extended-Spectrum B-lactamases (ESBL)?

A

-Hydrolyze narrow + extended spectrum-B-lactam antibiotics

-Hydrolyze most penicillins, cephalosporins, and monobactams

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50
Q

In which pathogens is the CTX-M enzyme of ESBLs most commonly found?

A

Escherichia coli

Klebsiella pneumoniae/oxytoca

Proteus mirabilis

51
Q

What are the treatments for ESBLs?

A

Carbapenems (meropenem, imipenem, doripenem, ertapenem)

Note that non-B-lactam antibiotics are an option depending on infection source and susceptibility

*Piperacillin/tazobactam are an option for urinary sources only

52
Q

What enzyme is an example of an Extended-spectrum B-lactamase (ESBL)?

A

CTX-M-15

53
Q

What is the function of Serine carbapenemases?

A

B-lactamase that hydrolyzes carbapenems

54
Q

What enzymes are examples of serine carbapenemases?

A

KPC-1
KPC-2
KPC-3

55
Q

What 6 pathogens is the KPC enzyme commonly found in?

A

-K. pneumoniae
-K. oxytoca
-E. coli
-E. cloacae
-E. aerogenes
-P. mirabilis

56
Q

What are the treatment options for Carbapenemase?

A

B-lactams: ceftazidime/avibactam, meropenem/vaborbactam, imipenem/cilastatin/relebactam
(B-lactam + B-lactam inhibitor)

Non-B-lactams: Plazomicin, Eravacycline, Omadacycline

57
Q

Which B-lactamase is considered Ambler Class B?

A

Metallo-B-lactamases

58
Q

What is the function of Metallo-B-lactamases?

A

Hydrolyze carbapenems

*confer resistance to all B-lactams except monobactams (aztreonam)

59
Q

What enzyme is an example of a Metallo-B-lactamase?

A

NDM-1

60
Q

What are the treatment options for Metallo-B-lactamases?

A

LIMITED -no B-lactamase inhibitors will work

-Cefiderocol

-Aztreonam + Ceftazidime/Avibactam

61
Q

Which B-lactamase is considered Ambler Class C?

A

Cephalosporinases

62
Q

What kind of resistance do cephalosporinases produce?

A

Inducible

63
Q

What enzyme is an example of a cephalosporinase?

A

Amp-C

64
Q

What are the 3 mechanisms of AmpC production?

A

**Inducible via chromosomally encoded AmpC genes
(if you put a patient on a drug that induces this then the patient gets worse)

Non-inducible chromosomal resistance via mutations (rare)

Plasmid-mediated resistance

65
Q

What pathogens is AmpC found in?

A

Hafnia alvei
Enterobacter cloacae
Citrobacter freundii
Klebsiella aerogenes
Yersinia enterocolitica
(HECK-Yes)

*these are the only bacteria that can induce AmpC, must know these for treatment

66
Q

What are the possible treatments for AmpC?

A

*Cannot use older B-lactamase inhibitors

*Can use newer ones: avibactam, vaborbactam, relebactam

67
Q

How is AmpC induced?

A

-Enzyme production increases in the presence of certain beta-lactam agents
-Initially, the gene for beta-lactamase production is REPRESSED, goes to an inducer, and the gene is DEREPRESSED, leading to increased beta-lactamase production
-Remove the inducer and the gene is repressed, beta lactamase production goes back to low levels
-Genetic mutation leads to the gene being derepressed, stable derepression, and high level beta-lactamase production continuously
-Different beta-lactams induce AmpC beta-lactamases to varying degrees

*see lec 2 slide 41+42

68
Q

Which drug is a weak inducer of AmpC and has a high susceptibility to AmpC hydrolysis?

A

Ceftriaxone

69
Q

What is a stably derepressed AmpC mutant?

A

Organism initially tests susceptible but then subsequently tests as resistant

-this occurs in 20-40% of cases treated with 3rd generation cephalosporins

70
Q

What is the treatment for stably derepressed mutants?

A

Cefepime

71
Q

JH is a 65 YOM admitted with pyelonephritis (infection in the kidney) and started on IV ceftriaxone.
However, he soon develops a fever and becomes hypotensive. Blood cultures are taken and result
for E. cloacae.
Q1)What could explain his sudden decompensation?

a) E. cloacae harbors an ESBL gene and this was induced with ceftriaxone treatment
b) E. cloacae harbors a KPC gene and this was induced with ceftriaxone treatment
c) E. cloacae harbors an AmpC gene and this was induced with ceftriaxone treatment
d) E. cloacae harbors a NDM gene and this was induced with ceftriaxone treatment

A

c) E. cloacae harbors an AmpC gene and this was induced with ceftriaxone treatment

72
Q

2) What antibiotic change do you recommend?

a) Switch to Piperacillin/tazobactam
b) Switch to Cefepime
c) Switch to Ceftazidime
d) Switch to Aztreonam

A

b) Switch to Cefepime

(see stably derepressed mutants)

73
Q

Which B-lactamase is considered Ambler Class D?

A

OXA-type

74
Q

What are the functions of OXA-type B-lactamases?

A

Hydrolyze:
-oxacillin
-oxyimino B-lactams
-carbapenems

*can ether hydrolyze a very broad or narrow range of beta lactams depending on which one it is

75
Q

What enzyme is an example of an OXA-Type B-lactamase?

A

OXA-48

76
Q

In which pathogens are OXA-type B-lactamases typically found?

A

Acinetobacter baumannii (A. baumannii)

Pseudomonas aeruginosa

77
Q

What are the treatment options for OXA-Type B-lactamases?

A

Limited

-Cefiderocol
-Sulbactam/durlobactam

78
Q

What are 4 important points to remember about Carbapenem Resistance?

A

-Resistance is associated with the loss of our safest last line of defense

-Cross resistance to other antibiotic classes is very prevalent

-Resistance can be due to beta-lactamase or non-beta-lactamase causes (porin channels, efflux pumps)

-Carbapenem-resistant Enterobacterales (CRE) does not mean carbapenemases are present

79
Q

JM is a 45 YOM admitted with fever, chills, urinary frequency and urgency. Blood cultures are collected and 12
hour after admission rapid diagnostic testing identifies E.coli, CTX-M (+) in 4/4 bottles.

Q1) What type of antibiotic resistance is present?
a) Non-CP CRE
b) ESBL
c) NDM
d) KPC

A

b) ESBL

80
Q

JM is a 45 YOM admitted with fever, chills, urinary frequency and urgency. Blood cultures are collected and 12
hour after admission rapid diagnostic testing identifies E.coli, CTX-M (+) in 4/4 bottles.

Q2) What is the recommended treatment option?
a) Meropenem
b) Meropenem/vaborbactam
c) Aztreonam + Ceftazidime/avibactam
d) Piperacillin/tazobactam

A

a) Meropenem

81
Q

Another source of enzymatic inactivation causing resistance is Aminoglycoside-Modifying Enzymes. This is the most common method of ___________ resistance.

A

aminoglycoside

82
Q

What are the 3 mechanisms by which resistance through aminoglycoside-modifying enzymes can occur?

A

Acetylation
Nucleotidylation
Phosphorylation

83
Q

How do aminoglycoside-modifying enzymes work?

A

Modify aminoglycoside structure by transferring the indicated chemical group to a specific side chain

(impairs cellular uptake and/or binding to ribosome)

84
Q

What is the mechanism of resistance of vancomycin in enterococci species?

A

Altered Target Site: Cell Wall Precursor

-vancomycin binds to D-alanine-D-alanine terminus of peptidoglycan precursors
-inhibits cell wall synthesis

*Resistance alters D-Ala-D-Ala to D-Ala-D-Lac or D-Ala-D-Ser

85
Q

What genes mediate vancomycin resistance through altered cell wall precursor?

A

VanA
VanB

86
Q

Vancomycin resistance through altered cell wall precursors, mediated by VanA and VanB, produces what?

A

Vancomycin-Resistant Enterococcus (VRE)

87
Q

What is the treatment for Cell Wall Precursor altered target site?
-vancomycin resistance

A

Daptomycin
Linezolid

88
Q

When Penicillin Binding Proteins (PBPs) become an altered target site, what happens?

A

B-lactam resistance

89
Q

Why do alterations in Penicillin Binding Proteins (PBPs) lead to B-lactam resistance?

A

Decreased affinity of PBPs for antibiotic

OR

Change in the amount of PBP produced by bacteria

90
Q

What gene causes B-lactam resistance due to alterations in Penicillin Binding Proteins (PBPs)?

A

mecA gene

91
Q

Besides B-lactam resistance, what else can the mecA gene indicate?

A

mecA+

means PBP2A+

means patient has MRSA
(methicillin-resistant staphylococcus aureus)

*PBP2A has resistance to B-lactams

92
Q

What is the treatment for mecA + resistance?

A

Ceftaroline
Ceftobiprole
Vancomycin
Daptomycin
Linezolid

93
Q

Alterations in PBP in Streptococcus pneumoniae can result in what?

A

Penicillin and Cephalosporin resistance

94
Q

What gene is responsible for Altered Ribosomal Target Sites?

A

ermB gene

95
Q

How can efflux pumps lead to resistance?

A

Efflux pumps actively transport antibiotics out of the periplasmic space

-overexpression leads to high-levels of resistance

96
Q

Efflux pump overexpression is an important resistance mechanism for what pathogens?

A

P. aeruginosa against carbapenems

S. pneumoniae against macrolide antibiotics

97
Q

How can porins cause resistance?

A

Porin channels are hydrophilic diffusion channels

-the rate of antibiotic diffusion depends on porin + antibiotic physiochemical characteristics

-smaller, more hydrophilic antibiotics pass through easier than large, hydrophobic ones

**Mutations can result in loss of specific porins which leads to antibiotic resistance

98
Q

Porin channel mutations that cause resistance are most commonly seen in which pathogens?

A

Enterobacterales

Carbapenem-resistant P. aeruginosa

99
Q

What is the mechanism of Staphylococcus aureus resistance to beta-lactams?

a) mecA gene
b) VanA gene
c) ermB gene
d) KPC gene

A

a) mecA gene

100
Q

What is Pharmacokinetics (PK)?

A

Process by which the drug enters and leaves the body based on ADME

101
Q

What is Pharmacodynamics (PD)?

A

Describes the biochemical and physiological response of the drug and its mechanism of action

102
Q

What is bactericidal?

A

KILLING of the organism by acting on areas such as the cell wall, cell membrane, bacterial DNA, etc

103
Q

What is bacteriostatic?

A

INHIBITING BACTERIAL REPLICATION without killing the organism by inhibiting protein synthesis

104
Q

What is the Cmax?

A

The highest drug concentration

(peak)

105
Q

What is the AUC?

A

Overall drug exposure over a certain time

106
Q

What is the MIC?

A

Minimum inhibitory concentrations

107
Q

What is the Post Antibiotic Effect (PAE)?

A

Continued growth inhibition for a variable period after the concentration at the site of infection has decreased below the MIC

108
Q

What does Concentration Dependent mean?

A

Maximize concentration at binding site

109
Q

What does Time Dependent mean?

A

Optimize duration of exposure at binding site

110
Q

What does a large Cmax/MIC mean?

A

Greater killing

*Correlates with increased area under the curve

111
Q

Which antibiotics have time-dependent PD?

A

All B-lactams
(penicillin, cephalosporin, carbapenem, monobactam)

*Vancomycin

112
Q

Which antibiotics have concentration dependent PD?

A

Fluroquinolones: Levofloxacin, Ciprofloxacin

Aminoglycosides: Gentamicin, Tobramycin, Amikacin

*Daptomycin

113
Q

The time that free drug concentration remains above MIC correlates with what?

A

Clinical and Microbiological outcomes

114
Q

For what percent of the time do we want the free drug concentration to be above the MIC in:
-Carbapenems
-Penicillins
-Cephalosporins

to maximize fT>MIC?

A

Carbapenems >/=40%
Penicillin >/= 50%
Cephalosporins >/=60%

115
Q

What are the strategies to maximize fT>MIC?
(free drug concentration > MIC)

A

Increase dose, same interval

Same dose, shorter interval

Continuous infusion

Prolonged infusion

116
Q

How is vancomycin’s PD different than other antibiotics?

A

Time-dependent bactericidal activity

Long post-antibiotic effect for gram-positive organisms

117
Q

What target is used for vancomycin PD?

A

AUC/MIC

Goal: 400-600

118
Q

What AUC/MIC is considered elevated and has a high risk of nephrotoxicity?

A

> /= 600-700

119
Q

Which of the following describes the PK/PD parameters of meropenem?

a) Time-dependent antibiotic; fT>MIC 40% of the dosing interval
b) Concentration dependent antibiotic; fAUC/MIC
c) Time-dependent antibiotic; fT>MIC 80% of the dosing interval
d) Concentration dependent antibiotic; Cmax/MIC

A

a) Time-dependent antibiotic; fT>MIC 40% of the dosing interval

120
Q

What are the predictive PK/PD parameters for aminoglycosides + Daptomycin?

A

Peak/MIC

AUC/MIC

121
Q

What are the predictive PK/PD parameters for B-lactams?

A

T>MIC

122
Q

What are the predictive PK/PD parameters for fluoroquinolones + vancomycin?

A

AUC/MIC

123
Q

Is vancomycin bacteriocidal or bacteriostatic?

A

Cidal (slowly)

Spring 2025 Therapeutics V (13 decks)

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